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Minipress (Prazosin)
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Minipress

Minipress is an effective strong preparation which is taken in treatment of hypertension diseases. Minipress is also helpful in treatment of male prostate enlargement symptoms, congestive heart failure, Raynaud's disease. Minipress acts as anti-hypertension remedy.

Other names for this medication:

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Lisinopril, Amlodipine, Norvasc, Benicar, Metoprolol, Hydrochlorothiazide, Avapro, Losartan

 

Also known as:  Prazosin.

Description

Minipress is created by pharmacy specialists to combat hypertension disease. Target of Minipress is to control level of blood pressure.

Minipress acts as anti-hypertension remedy. Minipress operates by reducing blood pressure.

Minipress is also known as Prazosin, Prazopress, Vasoflex, Hypovase.

Minipress is alpha blocker.

Generic name of Minipress is Prazosin (oral).

Brand name of Minipress is Minipress.

Dosage

You should take it by mouth with water.

It is better to take Minipress 2-3 times a day at the same time with meals or milk.

It is better to start the first Minipress dose when are going to bed.

If you want to achieve most effective results do not stop taking Minipress suddenly.

Overdose

If you overdose Minipress and you don't feel good you should visit your doctor or health care provider immediately. Symptoms of Minipress overdosage: feeling lightheaded, rash, weakness, troublesome breathing, pruritus, swelling.

Storage

Store at room temperature between 15 and 30 degrees C (59 and 86 degrees F) away from moisture, light and heat. Keep container tightly closed. Throw away any unused medicine after the expiration date. Keep out of the reach of children in a container that small children cannot open.

Side effects

The most common side effects associated with Minipress are:

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Side effect occurrence does not only depend on medication you are taking, but also on your overall health and other factors.

Contraindications

Do not take Minipress if you are allergic to Minipress components.

Be careful with Minipress if you're pregnant or you plan to have a baby, or you are a nursing mother.

Be careful with Minipress if you are taking any prescription or nonprescription medicine, herbal preparation, or dietary supplement.

Be careful with Minipress if you have allergies to medicines, foods, or other substances.

Be careful with Minipress if you have liver or kidney disease, heart failure, low blood pressure, narcolepsy, prostate cancer.

Be careful with Minipress if you take muscle relaxants as carisoprodol; anti-anxiety drugs as diazepam; anti-seizure drugs as carbamazepine; tranquilizers; sleep medicines as sedatives; antihistamines as diphenhydramine; verapamil; psychiatric medicines as tricyclic antidepressants (amitriptyline), phenothiazines (chlorpromazine); sexual function problems drugs as vardenafil, sildenafil, tadalafil; narcotic pain relievers as codeine; beta blockers as metoprolol, propranolol, atenolol.

Avoid machine driving.

Use Minipress with great care in case you want to undergo an operation (dental or any other).

Avoid alcohol.

Minipress can be not safety for elderly people.

Try to be careful with sunbeams. Minipress makes skin sensitive to sunlight. Protect skin from the sun.

Do not stop taking Minipress suddenly.

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Epinephrine and norepinephrine (1-10 microM) stimulated the release of prostacyclin (PGI2) from the rabbit aorta in vitro. The stimulation was maintained for at least 2 h in the continuous presence of epinephrine. Phenylephrine mimicked this effect, whereas the selective alpha 2-agonist UK-14,304 was completely ineffective. The action of epinephrine was abolished by prazosin (1 microM) and was maintained in the presence of yohimbine. Epinephrine or phenylephrine neither increased the basal release of PGI2 from bovine aortic endothelial cells nor potentiated the stimulatory action of adenine nucleotides, which is mediated by P2-purine receptors. The response to epinephrine was lost in freshly deendothelialized strips of rabbit aorta, possibly because of cyclooxygenase self-inactivation. The response recovered however following overnight incubation of these strips in a cell culture medium. The response to epinephrine was mimicked by neither phorbol 12-myristate,13-acetate nor ionophore A23187. It was not inhibited by pretreatment with pertussis toxin. It is concluded that adrenergic agents stimulate the vascular production of PGI2, by activating alpha 1-receptors located on smooth muscle cells.

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The number of membrane-bound beta-adrenoceptors is reduced in the myocardium of spontaneously hypertensive rats, and this decline may account for the decreased inotropic responsiveness to beta-agonists. It is not known, however, whether the total complement of cellular beta-receptors is lower in hypertensive animals. This issue was examined using two different approaches: acid elution of cell surface-bound beta-receptor ligands and comparison of the number of receptors in the plasma membrane and a postcytosolic vesicular fraction. Approximately 30% of the total beta-receptors were located intracellularly in Wistar-Kyoto rats compared with 42% for spontaneously hypertensive rats. Similarly, a decline in membrane-bound beta-receptors in hypertensive rats was balanced by a rise in receptors associated with the vesicular fraction. In contrast, alpha 1-adrenoceptors were higher in the membrane and lower in the vesicular fraction of hypertensive rats without a significant difference in total alpha-receptors compared with normotensive animals. Differences in adrenergic responsiveness in this, and perhaps other, models of cardiac hypertrophy reflect altered intracellular distribution of adrenoceptors, which may be under the control of the sympathetic nervous system.

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The purpose of this study was to evaluate the effects of carvedilol, a beta 1&2-adrenergic blocker and vasodilator, on cirazoline-mediated changes in arterial blood pressure and isoproterenol-mediated changes in heart rate after acute and chronic administration. Conscious, chronically instrumented male Sprague-Dawley rats were injected with carvedilol (1 mg/kg, IV), prazosin (0.3 mg/kg, IV), or propranolol (1 mg/kg, twice daily for 8 days. After administration of the first dose of carvedilol on day 1, the vasopressor response to cirazoline (60 +/- 3 mmHg predrug) and the isoproterenol-induced tachycardia (152 +/- 13 beats/min predrug) were blocked (e.g., 7 +/- 4 mmHg postdrug and 11 +/- 3 beats/min postdrug, respectively). After the administration of carvedilol on day 8, the cirazoline vasopressor response was 2 +/- 1 mmHg and the isoproterenol-induced tachycardia was 4 +/- 3 beats/min, indicating effective alpha 1- and beta-adrenergic blockade after chronic dosing with carvedilol. Prazosin blocked the cirazoline-induced vasopressor response on both days 1 and 8 but had no effect on the isoproterenol-induced tachycardia. Propranolol blocked the isoproterenol-induced tachycardia on both days 1 and 8 but had no effect on the cirazoline vasopressor response. These data indicate that only carvedilol effectively blocked both alpha- and beta-adrenergic hemodynamic responses and that the antagonism of these responses with carvedilol was not diminished after chronic dosing of twice-a-day treatment for 8 days.

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We investigated the effects of intraperitoneal administration of adrenoceptor antagonists to the hyperthermia and hyperglycemia induced by prostaglandin F2 alpha (50 micrograms) injected into the third cerebral ventricle in anesthetized rats. Phentolamine inhibited the hyperthermia and hyperglycemia induced by prostaglandin F2 alpha. Prazosin inhibited the hyperthermia induced by prostaglandin F2 alpha, while enhancing the hyperglycemia. Yohimbine inhibited the prostaglandin F2 alpha-induced hyperglycemia without an effect on the hyperthermia. Propranolol had no effect on either prostaglandin F2 alpha-induced hyperglycemia or hyperthermia. These observations suggest that the hyperglycemia induced by prostaglandin F2 alpha is regulated by alpha 2-adrenoceptor systems while the hyperthermia is regulated by alpha 1-adrenoceptor systems in rats.

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Adult female rats were treated with prazosin, a selective alpha 1-adrenoceptor inhibitor, for 60 days in doses of 0.5 mg/kg/day or 0.5 mg/kg/8 h. Prolonged prazosin administration lowered the gain of body weight and significantly decreased systolic blood pressure and heart weight. Prazosin administered every 8 h also lowered serum triglycerides but did not change the total cholesterol level. Selective alpha 1-inhibitor treatment increased the adrenal gland weight and decreased the number of adrenocortical cells; in every 8 h treated group this effect being connected with a marked cell hypertrophy (in all adrenocortical zones). Our results suggest that prazosin induced changes in the structure of the rat adrenal cortex depend on activation of the hypothalamo-pituitary-adrenocortical axis and possibly on the small inhibition of the proliferative activity of rat adrenocortical cells.

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CT (25 and 50 mg/kg) increased swimming activity (P<0.05) by 92.73% and attenuated immobility time by 35.72%, similar to anti-immobility effect of imipramine (33.87%) in FST. In addition, CT (50 mg/kg) significantly (P<0.01) reduced immobility time by 30.24% in TST. -However, the antidepressant-like effect elicited by CT was reversed by metergoline, cyproheptadine, and sulpiride (40.81, 45.93, and 48.52%, respectively) pretreatment but prazosin, and yohimbine failed to reverse this antidepressant-like effect. Similar to diazepam, CT (25 mg/kg) increased duration of open arms exploration (P<0.05) by 43.73% in EPM, number of head-dips (HBT) (90.32%), and time spent in the light compartment by 45.77% in light/dark test indicating anxiolytic-like effect. The anxiolytic-like effect of CT was reversed by flumazenil pretreatment.

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These cases are discussed with reference to the known effects of KB220Z including enhanced dopamine homeostasis and functional connectivity of brain reward circuitry in rodents and humans. Their understanding awaits intensive investigation involving large-population, double-blinded studies.

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In patients not responsive to antihypertensive treatment and concomitantly affected by impaired glucose metabolism, achievement of target BP was obtained in more than one third of cases after 16-week add-on treatment with doxazosin. Changes in glyco-lipidic parameters and reduction of 10-year CHD risk observed during the study, although of moderate extent, confirm the overall favourable effect of antihypertensive combinations including doxazosin.

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Bradykinin (100 pM to 1 microM) contracted the rabbit urinary detrusor in vitro. The sensitivity to bradykinin was about 1000 times higher than that to acetylcholine (ACh) on a molar basis. The contractile response to bradykinin was unaffected by atropine, diphenhydramine, FPL-55712, methysergide, prazosin or tetrodotoxin, indicating that the contraction was not mediated via the release of ACh, histamine, peptide leukotrienes, serotonin or catecholamine. The bradykinin-induced contraction was, however, inhibited by indomethacin (5 microM), a cyclooxygenase inhibitor. Caffeic acid (10 microM), a lipoxygenase inhibitor, did not affect the contraction. Bradykinin (1 nM to 100 nM) stimulated the release of prostaglandin E2 from the detrusor in a concentration-dependent manner, and the release was abolished by treatment with indomethacin (5 microM). Prostaglandin (PG) E2 contracted the urinary detrusor with an EC50 of about 0.1 microM. Adenosine 5'-triphosphate (ATP), a stimulator of PG synthesis, also contracted the muscle with an EC50 of about 100 microM. [14C]Arachidonic acid was converted to PGE2 and F2 alpha when it was incubated with the 700 X g supernatant of the muscle homogenate. However, neither bradykinin nor ATP stimulated the PG synthesis in the supernatant. These results showed that bradykinin and ATP did not affect the cyclooxygenase and/or PG degradation system. On the other hand, when the intact detrusor muscle was incubated with [14C]arachidonic acid, bradykinin and ATP stimulated the PG synthesis, and the stimulated synthesis was inhibited by indomethacin. Mepacrine, a phospholipase A2 inhibitor, more potently inhibited the bradykinin- and ATP-induced contractions than the ACh-induced one.(ABSTRACT TRUNCATED AT 250 WORDS)

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The PATHWAY-2 study, funded by the British Heart Foundation, randomised 335 patients with resistant hypertension (already treated according to guidelines) to sequentially receive 12 weeks of spironolactone (25-50 mg), bisoprolol (5-10 mg), doxazosin (4-8 mg modified release) and placebo. The study design allowed drug comparisons in each patient, with 230 patients completing all cycles. Results showed that spironolactone reduced home systolic BP by 8.70 mm Hg more than placebo (<0.001), 4.26 mmHg more than bisoprolol/doxazosin (<0.001), 4.03 mm Hg more than doxazosin (<0.001), and by 4.48 mm Hg more than bisoprolol. By the end of the trial, there would only be 15 patients considered eligible for renal denervation trials in uncontrolled hypertension. PATHWAY-2 will have significant implications for patient recruitment in to other trials.

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The alpha-1 adrenergic innervation of the human prostate has been studied using radioligand receptor binding methods and in vitro contractile experiments. The density of alpha-1 adrenergic binding sites is of the same order of magnitude as alpha-2 adrenergic and muscarinic-cholinergic (MCh) receptors in the human prostate adenoma. The contractile response of human prostate adenomas to selective alpha-1, alpha-2, and MCh agonists indicated that smooth muscle contraction of the human prostate is mediated by alpha-1 adrenoceptors. The selective affinities of terazosin for alpha-1 and alpha-2 binding sites were determined using competitive displacement assays. Terazosin was shown to have a four hundred-fold greater affinity for alpha-1 binding sites. The concentration of terazosin-inhibiting phenylephrine-induced contractions suggested that terazosin inhibits prostate smooth muscle contraction via alpha-1 adrenoceptors.

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We prospectively studied the effect of terazosin on bladder compliance in 12 spinal cord injured patients. All study patients had demonstrated previously poor compliance despite clean intermittent catheterization and maximum anticholinergic therapy. Patients were started on 5 mg. terazosin nightly for 4 weeks. They were evaluated with a history, physical examination, symptom score, and synchronous cystoscopy and cystometry before, during and after terazosin therapy. Detrusor compliance improved in all patients during the treatment phase. The change in bladder pressure and the safe bladder volume were statistically and clinically significant. Patients also reported fewer episodes of incontinence and dysreflexia. The improvement in compliance and continence suggests that in the spinal cord injured patient terazosin may have an effect on alpha receptors in the detrusor muscle or central effects and that improved compliance is not due to decreased outlet resistance.

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The adrenoceptor mechanism that mediates the reduction of urinary sodium (UNa V) and bicarbonate (UHCO3 V) excretion during 1.0-Hz renal nerve stimulation (RNS) was evaluated in 21 anesthetized dogs. In each animal RNS decreased UNa V and UHCO3 V without changing mean arterial pressure, renal blood flow, or glomerular filtration rate. After these initial responses, dogs were administered phentolamine [2.0 micrograms.kg-1.min-1 intrarenal artery (ira); n = 7], prazosin (0.7 micrograms.kg-1.min-1 ira; n = 5), (+/- )-propranolol (2.0 micrograms.kg-1.min-1 ira; n = 4), or atenolol (50 mg/kg iv; n = 5) and the renal responses to RNS were again tested. Both the antinatriuretic response and reduction of UHCO3 V during RNS were abolished by alpha 1/alpha 2-adrenoceptor blockade with phentolamine and by alpha 1-adrenoceptor antagonism with prazosin. beta-Adrenoceptor blockade with (+/- )-propranolol (beta 1/beta 2) or atenolol (beta 1) did not alter either the decrease in UNa V or UHCO3 V after RNS. These results provide further evidence that, during low-frequency RNS, reduction of UNa V is mediated in part by carbonic anhydrase-dependent bicarbonate reabsorption. These antinatriuretic responses and decreases in UHCO3 V during 1.0-Hz RNS are mediated by adrenergic neurotransmitter stimulation of alpha 1-adrenoceptors.

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Recent evidences from molecular biology, radioreceptor binding and functional studies indicate that the alpha 1-adrenoceptor population is heterogeneous and can at least be divided into two subclasses named alpha 1A and alpha 1B. The present study was designed to obtain, a selective enrichment of rat brain cortical membranes with each subtype of alpha 1-adrenoceptor using alkylating agents. [3H]prazosin binding to rat cortical membranes was saturable and of high affinity (KD = 0.11 +/- 0.02 nM; Bmax = 132.5 +/- 7.2 fmol/mg protein). All ligands competed for specific [3H]prazosin binding in a statistically significant biphasic manner (%Rhigh = 30-40%; %Rlow = 60-70%). These sites meet generally accepted and recently described pharmacologic criteria for their identification as the alpha 1A- and alpha 1B-adrenoceptors. After pretreatment of membranes with benextramine (1 microM) in the presence of clonidine (1 microM), the antagonists, WB4101, (+)-niguldipine and phentolamine, displaced the radioligand with an inhibition curve steeper than in control membranes and with Ki values that agree with those obtained for the low affinity site present in control membranes. On the other hand, after pretreatment with chloroethylclonidine (10 microM) in the presence of WB4101 (1 nM), Hill coefficients for the displacement of the radioligand by WB4101, (+)-niguldipine, and phentolamine, were also increased, but in contrast to the situation described above, the Ki values agree with those obtained for the high affinity site present in control membranes. In conclusion, this method of partial alkylation of receptors could be a valuable tool for separately studying the pharmacological characteristics of the alpha 1-adrenoceptor subtypes in native membranes of cerebral tissue.

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Consumption of cardiovascular drugs oscillated between 324 DDD/1000p/Day for drugs with action on the renin-angiotensin system, and 6.5 DDD/1000p/Day for anti-aldosterone diuretics. Variation in consumption for areas in the 5th and 95th percentiles went from 1.8 times (digitalics) to 17.2 times (flavonoids), although most of the groups showed an extremal quotient of around 5. Variation in average prices was lower than in consumption (1.1 times for doxazosin and 3.7 for flavonoids) and variations in pharmaceutical expenditure was similar to variation in consumption (from 2.0 timesfor digitalics to 13.0 times for flavonoids).

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An alkylating analog of prazosin, SZL49 [1-(4-amino-6,7-dimethoxy-2-quinazolinyl)-4-(2-bicyclo[2.2.2]octa-2,5- diene-2-carbonyl)-piperazine], was synthesized and its pharmacological properties examined. SZL49 competed with nanomolar potency at [3H]prazosin binding sites of rat tissues. Pretreatment of membranes with SZL49 (10 nM) followed by washing led to a reduction in [3H]prazosin binding without a change in the Kd of the remaining sites. However, preincubation even at a concentration of 1 microM, led to only a 50% reduction in binding. Higher concentrations of SZL49 in the preincubation mixtures increased the Kd of the remaining sites. Pretreatment of membranes with phenoxybenzamine led to greater than 80% reduction in these sites. Preincubating membranes with SZL49 together with prazosin prevented the loss of binding caused by SZL49 alone. Utilizing different buffers or altering the ratio of absolute amounts of SZL49 and receptors in the preincubations failed to increase the blockade of [3H]prazosin binding sites. SZL49 was injected i.p. into rats and 16 hr later membranes were prepared from tissues and [3H]prazosin saturation experiments were performed. Whereas Kd values in brain and heart were no different from controls, the Kd value of the remaining kidney binding sites was increased approximately 5-fold in test animals in contrast to in vitro experiments. Maximum binding values of heart were reduced significantly by approximately 42%. Maximum binding values of kidney and brain were reduced about 21 and 36%, respectively. In functional studies with isolated rat aorta, pretreatment with SZL49, followed by a 1.5 hr washout, shifted to the right in a dose-dependent manner the dose-response curves for phenylephrine and norepinephrine.(ABSTRACT TRUNCATED AT 250 WORDS)

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A comparative study of cholinergic and adrenergic mechanisms was performed on isolated circular muscle strips of the canine ileum, ileocolonic junction and colon. Cholinergic agonists evoked atropine sensitive contractions, which were most prominent in the colon. The presence of neostigmine to inhibit acetylcholinesterase did not alter the relative sensitivities of the tissues to acetylcholine. The different maximal contraction to cholinergic agents discriminates the colon from the ileum and the ileocolonic junction. Alpha adrenoceptor agonists produced greater contractions in the ileocolonic junction and only marginal contractions in the colon. Phentolamine completely and prazosin and yohimbine partially blocked the response of the ileocolonic junction to norepinephrine, suggesting the involvement of both alpha-1 and alpha-2 adrenoceptors. As in other sphincteric gut smooth muscle, the contractile effects of alpha adrenergic agents are more important than the inhibitory ones. The different effects of cholinergic and adrenergic agents on the ileocolonic junction, as compared sphincteric properties in the canine ileocolonic junction. sphincteric properties in the canine ileocolonic junction.

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The effect of a newly synthesized irreversible blocker of the alpha-1 receptor [1-(4-amino-6,7-dimethoxy-2-quinazolnyl)-4-(2-bicyclo[2,2,2] octa-2,5-dienylcarbonyl)-piperazine; SZL-49] has been evaluated in contractile studies in rabbit aorta and binding studies in aorta and brain. SZL-49 produced long lasting inhibition of norepinephrine-induced contractions which was apparent 21 hr after drug washout. The inhibition, which was dose and time dependent, was characterized by progressive shift to the right in the norepinephrine dose-response curve. The ED50 for norepinephrine was shifted from 10(-7) M to 8 X 10(-7), 3 X 10(-6), 1 X 10(-5) and 5 X 10(-4) M after incubation (30 min) and washout of increasing concentrations of SZL-49. Surprisingly, SZL-49, irrespective of the dose or incubation time, did not decrease the maximal response of aortic rings to norepinephrine. This resulted in a norepinephrine dose-response curve after SZL-treatment that is parallel to the control. SZL-49 had no effect on the spasmogenic actions of histamine, serotonin, KCl or CaCl2. In contrast to the inhibitory pattern seen with SZL-49, incubation with 10(-7) M phenoxybenzamine shifted the norepinephrine dose-response curve to the right in a nonparallel manner and significantly depressed the maximal response obtainable with norepinephrine. Incubation with 10(-6) M phenoxybenzamine for 30 min virtually abolished the response to norepinephrine. Phenoxybenzamine (10(-7) M) was without effect on aortic rings treated with a maximally effective dose of SZL-49. Prazosin weakly antagonized the contractile actions of norepinephrine observed after SZL-49 treatment, whereas yohimbine was without effect on these norepinephrine-induced contractions. In control binding studies [3H]prazosin bound to two classes of sites in both aorta and brain preparations. Affinities and densities for these sites were K1 = 67.5 pM, K2 = 309 pM; R1 = 38.2 fmol/mg, R2 = 46.47 fmol/mg in aorta and K1 = 29.6 pM, K2 = 182 pM; R1 = 6.6 fmol/mg and R2 = 30.4 fmol/mg in brain. Treatment with increasing amounts of SZL-49 (10(-10) to 10(-8) M) progressively reduced the number of [3H]prazosin sites without altering the affinity of the sites remaining. At 10(-7) M, SZL-49 eliminated completely all specific [3H]prazosin binding. Our results indicate that the site mediating norepinephrine contraction after treatment with SZL-49 does not possess the characteristics of an alpha-1 receptor and supports the hypothesis that a low affinity site for norepinephrine and prazosin exists in vascular smooth muscle.(ABSTRACT TRUNCATED AT 400 WORDS)

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The main objective of this study was to characterize the alpha 1-adrenoceptors expressed in adult rat brown adipocytes. For this purpose, membrane fractions were prepared from brown adipose tissue as well as from isolated brown adipocytes. The following are major findings: (i) BAT membranes were considerably enriched in alpha 1-adrenoceptors (specific [3H]prazosin binding, Bmax, 79.49 +/- 16.77 fmol/mg protein; KD, 0.24 +/- 0.04 nM); (ii) among the cells that comprise brown adipose tissue, brown adipocytes were enriched in alpha 1-adrenoceptors; (iii) > 95% of total alpha 1-adrenoceptors were resistant to inactivation by 20 microM chloroethylclonidine, which readily and essentially completely inactivated alpha 1B-adrenoceptors in rat liver membranes; (iv) brown adipose tissue membrane alpha 1-adrenoceptors showed high affinity towards 5-methyl urapidil (KD 7.23 +/- 2.49 nM) and WB 4101 (KD 0.66 +/- 0.30 nM) and low affinity towards BMY 7378 (KD 0.34 +/- 0.03 microM); essentially similar affinities for these drugs were seen for membranes prepared from brown adipocytes; and (v) EBDA/LIGAND analysis of 5-methyl urapidil, WB 4101, and BMY 7378 competition curves revealed the presence of a single binding site for these drugs. Recent work has documented that 5-methyl urapidil and WB 4101 interact with high affinity with alpha 1A-adrenoceptors, while BMY 7378 interacts with high affinity with alpha 1D-adrenoceptors. Taken together, these findings are consistent with the view that alpha 1-adrenoceptors expressed in adult rat BAT are mainly of the alpha 1A subtype.

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Melatonin, the major secretory product of pineal gland has been suggested to play a regulatory role in the circadian rhythm of body activities including the pain sensitivity. Three subtypes of melatonin receptors, i.e. ML1, ML2 and ML3 have been identified.

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In order to characterize the hemodynamic actions of urotensin I, a vasodilator peptide with selectivity for the mesenteric vascular bed, we studied its hypotensive effects and interference with alpha-1 and alpha-2 adrenergic vasoconstrictor responses in the rat. After i.v. administration in anesthetized rats, urotensin I (0.06-6 nmol/kg) produced a dose-dependent lowering of arterial blood pressure. At hypotensive doses, urotensin I was about 3 times more potent in antagonizing systemic pressor responses to the selective alpha-1 adrenoceptor agonist, phenylephrine, than responses to the nonselective adrenoceptor agonist, norepinephrine. Additional studies were performed on the blood-perfused mesenteric bed of the anesthetized rat and on the isolated rat superior mesenteric artery, using as tools phenylephrine, norepinephrine and the relatively selective alpha-2 adrenoceptor agonist, alpha-methylnorepinephrine. The selectivity of the three agonists for vascular alpha-1 and alpha-2 adrenoceptors in the blood-perfused mesenteric bed was confirmed using prazosin and yohimbine as selective antagonists of alpha-1 and alpha-2 adrenoceptors, respectively. Urotensin I diminished the maximum increase in perfusion pressure and shifted the log dose-response curves to the right for all three agonists. A marked selectivity of urotensin I for alpha-1 adrenoceptor-mediated responses was observed: IC30 values of the peptide for pressor responses to phenylephrine, norepinephrine and alpha-methylnorepinephrine were 0.05, 0.83 and greater than 6 nmol/kg, respectively. A less pronounced selectivity of urotensin I for alpha-1 adrenoceptor-mediated contractions could be demonstrated in isolated strips of the superior mesenteric artery of the rat.(ABSTRACT TRUNCATED AT 250 WORDS)

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Alpha1-adrenergic receptors were quantified by radioligand binding assays, employing [3H]-prazosin as the radioligand in association with compounds displaying different degrees of selectivity for alpha1A-, alpha1B- and alpha1D-adrenergic receptor subtypes.

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Clonidine, an alpha 2-agonist, had a significant (P < 0.05) anti-secretory effect, while yohimbine, an alpha 2-antagonist, significantly (P < 0.05) increased net fluid secretion. Phenylephrine, an alpha 1-agonist, and prazosin, an alpha 1-antagonist, lacked significant effects on net fluid transport. Similarly, prenalterol, a beta 1-agonist, and metoprolol, a beta 1-antagonist, had no significant effect on the net fluid transport. The beta 2-agonist salbutamol significantly (P < 0.001) decreased net fluid secretion, while the beta-antagonist propranolol significantly (P < 0.001) decreased net fluid secretion.

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Naftopidil, an alpha 1-adrenergic antagonist, was orally tested in comparison with prazosin, in a rat cystomanometric model to evaluate the effect on the bladder volume capacity (BVC), the micturition pressure (MP) and the mean arterial blood pressure (MAP), contemporaneously recorded to evaluate the selectivity of action. Naftopidil induced a clearcut increase of BVC and a decrease of MP without lowering MAP at 6.25 mg kg-1 p.o.. Prazosin was inactive on BVC, decreased MP and induced a significant decrease of MAP at 1.56 mg kg-1 p.o. Naftopidil could offer an advantage when compared with prazosin.

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We have shown that, within therapeutic plasma concentrations, the unbound fraction of furosemide changes in direct proportion to the reciprocal of the plasma albumin concentration (correlation coefficient 0.99). Changes in the albumin concentration were produced by ultrafiltration of human plasma using a haemofiltration filter. Thus, we propose that, when studying changes in the pharmacokinetics of a highly protein bound drug, calculated changes in the unbound fraction offer an alternative to actual measurement of the unbound concentration, which is often difficult. Nine healthy volunteers receiving a continuous furosemide infusion were studied in normovolaemia and after dehydration (-1.4 kg), with and without pretreatment with an angiotensin converting enzyme inhibitor (captopril) or an a1-adrenoceptor blocking agent (prazosin). Significantly larger changes in the renal clearance of furosemide were found that could be explained by changes in the unbound fraction. Following dehydration, the unbound fraction of furosemide was decreased by about 5%, while its renal clearance fell by 27%, 33% and 13% after pretreatment with placebo, captopril and prazosin, respectively. The secretory clearance of the unbound furosemide changed substantially and in parallel with changes in the renal blood flow. It is suggested that changes in the renal clearance and excretion of furosemide and its t1/2 are much more dependent on changes in renal blood flow than on changes in its unbound fraction.

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All the patients got complete volume expansion after taking phenoxybenzamine with tachycardia occurring in 23 of them and postural hypotension in 13 patients. In the 25 cases mainly with increase of norepinephrine before medical treatment doxazosin mosylate was completely effective in 18 cases with their blood pressure < 180/140 mm Hg; and was partially effective in the other 7 cases with their blood pressure > 180/140 mm Hg of which 2 suffered from postural hypotension. Doxazosin mosylate was partially effective in the other 13 cases mainly with increase of both norepinephrine and epinephrine. The total efficiency rate of these two medicines was not significantly different (chi(2) = 18.05, P > 0.05). The side-effect rate of doxazosin mosylate was significantly lower than that of phenoxybenzamine (chi(2) = 324, P < 0.01).

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The present study was undertaken to investigate the effect of the ethanolic extract of Allium sativum L. (Family: Lilliaceae), commonly known as garlic, on depression in mice.

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The aim of the present study was to investigate dopamine receptor- and alpha-adrenergic receptor-mediated modulation of norepinephrine release in human atria. Right atrial appendages were incubated with 3H-norepinephrine, placed in superfusion chambers, and field-stimulated by platinum electrodes at a frequency of 5 Hz. The stimulation-induced (S-I) outflow of radioactivity was taken as an index of norepinephrine release. The dopamine D2-receptor agonist quinpirole (0.03-3 microM) concentration dependently inhibited the S-I outflow of radioactivity with an EC50 of 0.03 microM. The concentration-response curve of quinpirole was potently shifted to the right by the D2-receptor antagonists domperidone (0.003 microM, pKB approximately 9.2) and S(-)-sulpiride (0.1 microM, pKB approximately 8.6). The D1-receptor antagonist SCH 23390 (1 microM) slightly (pKB approximately 6.9) shifted the concentration-response curve of quinpirole, whereas the alpha 2-adrenergic antagonist rauwolscine (0.01 microM) and the alpha 1-adrenergic antagonist prazosin (1 microM) had no effect. The D1-receptor agonist did not affect fenoldopam (0.03 and 0.3 microM), but fenoldopam (3 microM) enhanced the S-I outflow of radioactivity. The facilitatory effect of fenoldopam (3 microM) was unaltered by SCH 23390 (0.1 microM) but prevented by rauwolscine (0.01 microM). The alpha 2-adrenergic agonist UK 14304 (0.01-1 microM) (EC50: 0.06 microM), but not the alpha 1-adrenergic agonist methoxamine (0.3-30 microM), inhibited S-I outflow of radioactivity. The concentration-response curve of UK 14304 was shifted to the right by rauwolscine (0.01 microM, pKB approximately 8.6).(ABSTRACT TRUNCATED AT 250 WORDS)

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minipress reviews 2017-08-20

Neuroleptics are known to stimulate dopamine release in neostriatal terminal areas. In the present study, we have investigated by brain microdialysis in freely moving rats the effect of typical and atypical neuroleptics on dopamine transmission in the bed nucleus of stria terminalis, a dopamine terminal area belonging to the limbic system and recently assigned the so-called extended amygdala. Mean basal dialysate dopamine values were 14.3 f moles/20 microliters sample. Dopamine output in dialysates was increased dose-dependently by clozapine (max + 158%, 298%, and 461% of basal at 5, 10, and 20 mg/kg i.p., respectively), risperidone (max + 115% and 221% of basal at 1 and 3 mg/kg i.p., respectively), olanzapine (max + 138% and 235% of basal at 3 and 6 mg buy minipress /kg i.p., respectively), BIMG 80 (max + 64% and 164% of basal at 3 and 5 mg/kg i.p., respectively), amperozide (max + 110% and 194% of basal at 3 and 6 mg/kg i.p., respectively). The selective dopamine D4 antagonist L-745,870 increased dialysate dopamine but at rather high doses and not as effectively as clozapine (max + 32%, 89%, and 130% of basal at 2.7, 5.4, and 10.8 mg/kg i.p., respectively). The typical neuroleptic haloperidol (0.1 and 0.5 mg/kg s.c.) and the selective D2 antagonist raclopride (0.14, 0.56, and 2.1 mg/kg s.c.), the serotonergic 5-HT2 antagonist ritanserin (0.5 and 1.5 mg/kg i.p.), and the adrenergic alpha 1 antagonist prazosin (0.91 and 2.73 mg/kg i.p.) did not affect dialysate dopamine in the bed nucleus of stria terminalis. Saline (1 ml/kg s.c. or 3 ml/kg i.p.) did not modify dialysate dopamine. Therefore, atypical neuroleptics share the ability of stimulating dopamine transmission in the bed nucleus of stria terminalis, but this property is not mimicked by any of the drug tested that selectively act on individual receptors among those that are affected by atypical neuroleptics. These observations raise the possibility that the property of increasing dopamine transmission in the bed nucleus of stria terminalis is the result of combined blockade of dopamine, serotonin, and noradrenaline receptors and that might be predictive of an atypical neuroleptic profile.

minipress user reviews 2015-11-19

Abnormal nocturnal blood pressure (BP) dipping status may be partly determined by nocturnal sympathetic activity. We studied the effect of nighttime dosing of an alpha(1)-adrenergic blocker, doxazosin, on the BP dipping status of 118 hypertensives, all of whom underwent 24-hour ambulatory BP monitoring before and after treatment. The mean nighttime/daytime ratio of systolic BP was increased (0.91 after therapy versus 0.89 at baseline, P<0.05). The patients were initially divided into 4 groups on the basis of their dipping status at the baseline assessment: 18 (15%) were extreme dippers, with a nighttime systolic BP fall of at least 20% of daytime BP; 46 (39%) were dippers (fall between 10% and 20%); 48 (41%) were nondippers (fall between 0% and 10%); and 6 (5%) were risers (nocturnal increase of systolic BP). A shift in dipping status toward less nocturnal BP dipping was observed after doxazosin therapy (P<0.05). Dipping status was determined by nighttime more buy minipress than by daytime BP, and this was not explained by differences in the number of daytime and nighttime readings. The effects of doxazosin on the mean nocturnal systolic BP changes were an increase of 4.3 mm Hg in extreme dippers and decreases of 0.7 mm Hg in dippers, 12 mm Hg in nondippers, and 18 mm Hg in risers; the reduction was only significant in the latter 2 groups (both P<0.01). To estimate the effects of regression to the mean on the changes in dipping status, we also defined dipping status with the average of the BPs before and after doxazosin and found no difference in the degree of nighttime BP reduction among each group. The reduction of daytime BP was now significantly greater in the subgroups with less dipping: 6. 4 mm Hg for extreme dippers and 16 mm Hg for risers (P<0.05). In conclusion, nighttime dosing with doxazosin markedly affects the nocturnal BP dipping status of hypertensives, but the apparently greater reduction in nighttime pressure in nondippers and risers may be, at least partly, due to the effect of regression to the mean. The most important determinants of the effect of doxazosin were the absolute BP levels, both day and night, rather than dipping status per se.

minipress capsules 2016-10-10

Raynaud's disease is characterized by excessive cutaneous vasoconstriction in response to ambient cold. A functional disturbance in the local regulation of digital vasomotion has been proposed. The purpose of this study was to determine whether there is an alteration in the postjunctional adrenergic receptors in the digital circulation of patients with Raynaud's disease. Furthermore, we sought to determine whether this abnormality was responsible for the excessive cold-induced vasoconstriction in these patients. Finger blood flow was buy minipress measured by strain-gauge venous occlusion plethysmography in 10 patients with Raynaud's disease and in 10 normal volunteers in a 22 degrees C room. Measurements of finger blood flow and mean systemic arterial pressure were made during intra-arterial infusions of the alpha 1-adrenergic antagonist, prazosin, or the alpha 2-adrenergic antagonist, yohimbine, at room temperature and during local cooling of the hand. Basal finger blood flow in normal subjects was significantly greater than that of patients (8.6 +/- 2.7 vs 1.7 +/- 0.5 ml/100 ml per min; normal vs Raynaud's subjects; p < 0.05). In normal subjects, either prazosin or yohimbine induced dose-dependent increases in finger blood flow. The maximal increase in finger blood flow induced by prazosin was significantly greater than that in response to yohimbine (29.2 +/- 10.1 vs 2.8 +/- 2.1 ml/100 ml per min; prazosin vs yohimbine; p < 0.05). By contrast, in the Raynaud's patients, prazosin or yohimbine induced maximal increases in finger blood flow that were not significant (7.1 +/- 1.8 vs 5.0 +/- 2.2 ml/100 ml per min; prazosin vs yohimbine; p = NS). The response to prazosin in Raynaud's patients was significantly less than that of the normal volunteers (p < 0.05). In normal subjects, during intra-arterial infusion of vehicle alone, cooling induced a 52.6 +/- 5.8% reduction in finger blood flow. This cold-induced vasoconstriction was blunted, but not qualitatively altered, by either adrenergic antagonist. In the Raynaud's patients, during the intra-arterial infusion of the vehicle, cooling induced a 68.2 +/- 7.8% reduction in finger blood flow. Infusion of either adrenergic antagonist blunted, but did not qualitatively alter, the response to cold. Finger blood flow is less in patients with Raynaud's disease than in normal subjects when studied in a 22 degrees C room. In normal subjects, postjunctional alpha 1-adrenergic receptors appear to predominate in the control of digital vasoconstriction. Postjunctional alpha 1- and alpha 2-adrenoceptors play an equal role in adrenergic regulation of finger blood flow in patients with Raynaud's disease. In both normal and Raynaud's subjects, selective antagonism of alpha 1- or alpha 2-adrenergic receptors does not abolish local cold-induced vasoconstriction. Therefore, it is likely that a nonadrenergic mechanism contributes to local cold-induced vasoconstriction.

minipress xl tablets 2017-02-18

This study investigated the antinociceptive mechanisms of khat extract (100, 200, and 400 mg/kg, i.p.) in four pain models: two thermic (hot plate, tail-flick) and two chemical (acetic acid, formalin) models. Male mice were pretreated intraperitoneally (i.p.) with the opioid receptor blocker naloxone (5 mg/kg), the cholinergic antagonist atropine (2 mg/kg), the selective α1 buy minipress blocker prazosin (1 mg/kg), the dopamine D2 antagonist haloperidol (1.5 mg/kg), or the GABAA receptor antagonist, bicuculline (1 mg/kg) 15 minutes prior to i.p. injection of khat extract (400 mg/kg). Khat extract reduced the nociceptive response of mice in the four pain tests. Naloxone significantly inhibited the antinociceptive effect of khat extract in the hot plate, tail-flick, and the first phase of formalin tests. Bicuculline significantly antagonized the antinociceptive effect of khat extract on the hot plate and tail-flick tests. Haloperidol significantly reversed the antinociceptive effect of khat extract on the tail-flick test and the first phase of formalin test. These results provide strong evidence that the antinociceptive activity of khat extract is mediated via opioidergic, GABAergic, and dopaminergic pathways. The mechanism of the antinociceptive action of khat may be linked to the different types of pain generated in animal models.

minipress 2 mg 2017-12-16

We have studied the role of alpha 1A- and alpha 1B-adrenoceptors in noradrenaline- and methoxamine-stimulated inositol phosphate accumulation in rat renal cortical slices. [3H]Prazosin binding studies with and without inactivation of alpha 1B-adrenoceptors by chloroethylclonidine treatment suggested that noradrenaline lacks relevant selectivity for alpha 1-adrenoceptor subtypes. Both agonists stimulated [3H]inositol phosphate accumulation with similar maximal effects. The alpha 1A-selective antagonists 5-methyl-urapidil and (+)-niguldipine inhibited inositol phosphate formation by both agonists with shallow biphasic curves but the high affinity component was only 15%-31% and 38%-41%, respectively. The irreversible alpha 1B-selective antagonist chloroethylclonidine inhibited inositol phosphate generation by both agonists by 54%-57%. In contrast to our previous buy minipress data in rat cerebral cortical slices, we conclude that in rat renal cortex both alpha 1A- and alpha 1B-adrenoceptors are involved in noradrenaline- and methoxamine-stimulated inositol phosphate generation.

minipress nightmares dosage 2016-07-31

Phenoxybenzamine, prazosin, WB-4101, chloroethylclomidine and buy minipress yohimbine all inhibit the contractile response of the rat seminal vesicle to electrical nerve stimulation. As phenoxybenzamine is effective in treating premature ejaculation, the comparable in vivo potencies of WB-4101 and yohimbine strongly suggest that they have clinical therapeutic potential.

minipress overdose 2017-07-21

Suburothelial venules showed spontaneous action potential and vasoconstriction activity while suburothelial arterioles were quiescent. Venular vasoconstriction was prevented by cyclopiazonic acid or nicardipine and decreased by 2-aminoethoxydiphenyl borate, niflumic acid or 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid. Venular smooth muscle cells and perivascular interstitial cells showed buy minipress spontaneous Ca(2+) transients. Nicardipine decreased the amplitude and disrupted the synchronicity of Ca(2+) transients in and between the 2 cell populations. Residual Ca(2+) transients in nicardipine occurred asynchronously and were abolished by cyclopiazonic acid. Suburothelial arterioles constricted in response to transmural nerve stimulation. These nerve induced constrictions were suppressed by prazosin or the selective α(1A) blocker RS17053 but not by the α(1D) blocker BMY7378. Remaining constrictions were abolished by guanethidine.

minipress overdose symptoms 2016-08-06

Male mice were administered either prazosin, betaxolol, atipamezole, corticosterone, or repeated buy minipress restraint stress prior to measurement of either nest-leaving or TST. General behavioral function was assessed in horizontal wire, swim, and latency to escape footshock tests.

tab minipress dosage 2015-11-05

Overall, this study showed terazosin to be safe and effective in relieving the signs and buy minipress symptoms of BPH and should be considered as a treatment alternative.

minipress and alcohol 2016-12-19

Prospective study. buy minipress

minipress tab 2015-03-13

The results provide evidence for two apical membrane adrenergic receptors, alpha(1) and ss, activated by epinephrine and isoproterenol, respectively. The membrane voltage and resistance changes produced by these two agonists buy minipress mimic those produced by elevating [Ca(2+)](i) and [cAMP](i), suggesting that these ubiquitous signaling molecules activate separate basolateral membrane Cl channels inhibited by DIDS and NPPB, respectively. These two receptors, the apical membrane NaK2Cl cotransporters and the basolateral membrane Cl channels form a complex of proteins that help mediate fluid absorption across human RPE.

minipress medication 2016-03-10

On the basis of both radioligand and functional studies, the existence of a novel receptor that was unique from the alpha 2-adrenoceptor has become evident. Our initial studies contrasted the function of I1 imidazoline receptor agonists with that of purported alpha 2-adrenoceptor agonists in the kidney. The mechanism by which urine flow increased (osmolar vs free water clearance) as well as the effects of idazoxan, rauwolscine, a V2 vasopressin receptor antagonist, indomethacin pretreatment, and one-kidney one clip hypertension in rats were different following moxonidine when compared to an alpha 2-adrenoceptor agonist. This indicated two separate receptor systems. Subsequent studies determined that i.c.v. administration of moxonidine would also increase the urine flow rate by increasing osmolar clearance. This response to i.c.v. moxonidine differed from the response of an alpha 2-adrenoceptor agonist administered i.c.v.. Moreover, this effect of i.c.v. moxonidine was unique from that observed following the intrarenal infusion of moxonidine (Fig. 2). Denervation, intravenous prazosin, and i.c.v. idazoxan selectively blocked the effects buy minipress of i.c.v. moxonidine. Intravenous idazoxan selectively blocked the response to intrarenal infusion of moxonidine. On the basis of the response to i.c.v. moxonidine in SH rats, the site(s) and/or receptor(s) responsible for blood pressure lowering were altered and those for increasing sodium excretion appear to be inactive. The significance of the findings in long-term regulation of blood pressure remain to be determined.

minipress drug class 2016-10-14

Radioligand receptor binding methods were used to characterize the alpha 1-adrenergic receptor in the bladder body, bladder base, prostate and urethra of the male dog. Saturation experiments were performed in tissue homogenates using [125iodine]-Heat, an alpha 1-adrenergic antagonist of high specific activity (2,200 Ci. per mmol.). The equilibrium dissociation constant Kd for [125iodine]-Heat binding in the bladder body (0.56 pM.), bladder base (0 buy minipress .81 +/- 0.11 pM.), prostate (0.86 +/- 0.19 pM.) and urethra (0.55 pM.) was similar, suggesting homogeneity of alpha 1-adrenergic binding sites in lower genitourinary tissues. The receptor density in the bladder body, bladder base, prostate and urethra, expressed as fmol. per mg. wet weight, was 0.22 +/- 0.02, 0.82 +/- 0.09, 0.55 +/- 0.06 and 0.27 +/- 0.06, respectively (mean +/- standard error of mean). Competitive binding experiments with [125iodine]-Heat and unlabeled prazosin and clonidine confirmed the selectivity of Heat for alpha 1-adrenergic binding sites. Anatomical dissections have revealed that a major component of the smooth muscle of the bladder base and prostate originates from the ureter, whereas a major component of the smooth muscle of the urethra originates from the bladder. The measured alpha 1-adrenergic receptor densities support these developmental theories.

minipress xl dosage 2016-03-06

Pituitary tumors are common and cause considerable morbidity due to local invasion and altered hormone secretion. Doxazosin (dox), a selective alpha(1)-adrenergic receptor antagonist, used to treat hypertension, also inhibits prostate cancer cell proliferation. We examined the effects of dox on murine and human pituitary tumor cell proliferation in vitro and in vivo. dox treatment inhibited proliferation of murine pituitary tumor cells, induced G(0)-G(1) cell cycle arrest, and reduced phosphorylated retinoblastoma levels. In addition, increased annexin-fluorescein isothiocyanate immunoreactivity and cleaved caspase-3 levels, in keeping with dox-mediated apoptosis, were observed in the human and murine pituitary tumor cells, and dox administration to mice, harboring corticotroph tumors, decreased tumor growth and reduced plasma ACTH levels. dox-mediated antiproliferative and proapoptotic actions were not confined to alpha-adrenergic receptor-expressing pituitary tumor cells and were unaffected by cotreatment with the alpha-adrenergic receptor blocker, phenoxybenzamine. dox treatment led to reduced phosphorylated inhibitory kappaB (IkappaB)-alpha expression, and nuclear factor-kappaB transcription and decreased basal and TNFalpha-induced proopiomelanocortin transcriptional activation. These results demonstrate that the selective alpha(1)-adrenergic receptor Cymbalta Dosage Increase antagonist dox inhibits pituitary tumor cell growth in vitro and in vivo by mechanisms that are in part independent of its alpha-adrenergic receptor-blocking actions and involve down-regulation of nuclear factor-kappaB signaling. dox is proposed as a possible novel medical therapy for pituitary tumors.

minipress tablets dose 2016-07-03

1. The alpha 1-adrenoceptors present in membranes of rat liver, cortex and submaxillary gland were labelled with [3H]-prazosin and the affinity of 15 ligands for these receptors was determined. 2. In saturation studies, [3H]-prazosin bound with high affinity (Kd = 30-39 pM) to a single population of sites in all three preparations. 3. In competition studies using rat cortex, evidence for heterogeneity of the alpha 1-adrenoceptor binding sites was obtained. Displacement isotherms for amidephrine, benoxathian, oxymetazoline, phentolamine and WB 4101 Imodium Prescription Dose were biphasic and were consistent with the presence of both alpha 1A- and alpha 1B-adrenoceptor subtypes as described by Morrow & Creese (1986) and Han et al. (1987). 4. The rat liver and submaxillary gland membrane preparations both possessed homogeneous populations of alpha 1-adrenoceptors. However, there were pharmacological differences between the receptors in these two preparations. Rat submaxillary gland alpha 1-adrenoceptors displayed high affinity for amidephrine, benoxathian, oxymetazoline, phentolamine and WB 4101 and therefore appeared to represent alpha 1A-adrenoceptors. Rat liver alpha 1-adrenoceptors possessed lower affinity for these ligands (6-65 fold) suggesting that these receptors were of the alpha 1B-subtype. 5. Spiperone exhibited 12.9 fold higher affinity for rat liver alpha 1B-adrenoceptors than for rat submaxillary gland alpha 1A-adrenoceptor and may therefore represent the first alpha 1B-adrenoceptor selective ligand.

minipress cost 2015-12-12

Adrenergic and purinergic compounds contract the longitudinal muscles of the rat vas deferens. Whereas ATP and related purinergic analogs produced contractions of greater magnitude in the prostatic half as compared to that of the epididymal end, the magnitude of the alpha 1-adrenoceptor-induced responses was larger in the epididymal than in the prostatic half of the rat ductus. Chemical sympathectomy following a 48 hr 6-hydroxydopamine-treatment (6-OHDA) caused a leftward displacement of the concentration Cleocin 300 Mg -response curves for adrenergic and purinergic drugs, this effect being more evident in the prostatic segment. Sympathectomy caused a significant increase in the maximal response induced by ATP and adrenergic compounds which was more evident in the prostatic half of the rat ductus. The denervation-induced supersensitivity was stimulus-specific since angiotensin II and acetylcholine showed no significant change in potency. In the case of bradykinin, there was a manifest increase in the maximal response of the prostatic segment of the ductus of the chemically denervated tissues. In addition, denervation also caused an increase in the potency of prazosin and phentolamine as alpha 1-adrenoceptor blocking agents; denervation did not change the potency of yohimbine as an alpha 2-adrenoceptor blocker.

minipress tablets 2017-09-29

(dl)-(5 alpha,8 alpha,9 alpha)-5,8,9,10-Tetrahydro-5,9- methanobenzocycloocten-8-amine hydrochloride (Org 6906) is a potential new antidepressant agent, with a neurochemical profile quite different from that of the classical tricyclic antidepressant drugs. The compound was found active in behavioural tests which are considered to be predictive for antidepressant activity, such as the muricidal test in the rat and the acquired immobility model. Neurochemical studies showed that Org 6906 was an inhibitor of the reuptake of monoamines both in vitro and ex-vivo without having appreciable anticholinergic, antihistaminergic or alpha 1-adrenolytic activity. The facilitatory effect on monoaminergic neurotransmission was confirmed by the reversal of hypothermia induced by reserpine. The drug Org 6906 appeared to have selective alpha 2-adrenolytic properties. It facilitated potassium-stimulated release of noradrenaline from slices of cortex, displaced [3H]rauwolscine and [3H]dihydroergocryptine from their binding sites but only weakly blocked alpha 1-adrenoceptors. The alpha 2-adrenolytic properties were also apparent in behavioural interaction models. The compound antagonized the sleep-inducing effects of clonidine in chicks and mice and it antagonized the mydriasis induced by clonidine in Altace Medication Information the rat. Finally, it was shown that the two enantiomers of Org 6906 contributed almost equally to the relevant neurochemical and behavioural properties.

minipress drug interactions 2016-04-22

Compared with non-MEN patients, MEN2 patients were younger at diagnosis, had less symptoms, lower hormone levels, and smaller tumors. Intraoperatively, MEN2 patients had a similar frequency of hypertensive episodes (1.3 vs 1.9, P=0.162, 95% confidence interval (CI): -6.7 to 35.4) and a similar maximum SABP (200 vs 220  mmHg, P=0.180, 95% CI: -9.7 to 50.5). However, MEN2 patients experienced less frequent (1.04 vs 2.6, P=0.003, 95% CI: 0.57 to 2.6) and less severe hypotensive episodes after tumor resection (lowest MABP: 52.5 vs 45.6  mmHg, P=0.015, 95 Luvox Generic Name % CI: -12.6 to 1.16). Tumor size was an independent risk factor for HD instability for the total group after multivariate analysis.

minipress 4 mg 2015-08-26

Lysosomes, isolated from rat liver after 70% partial hepatectomy (PHX), were found, by Western blotting, to contain a considerable amount of serum albumin. The level of intralysosomal serum albumin after PHX showed biphasic patterns: it increased immediately after PHX, peaked at 30 min, rapidly declined within a few hours, rose again with a peak at 15 hr, and gradually declined thereafter. At 15 hr after PHX, the content of lysosomal proteins in the liver increased to twice the level of unoperated control, and the electron-microscopic observation of the isolated lysosomes revealed numerous large membrane-delimited structures with ground substances of variable electron opacities. The increase in the intralysosomal serum albumin at 30 min and 15 hr was accompanied by changes in the buoyant densities of endosomes in Percoll density gradients. At both time points, the density profiles of endosomes isolated from hepatectomized rats shifted to the denser direction, suggesting that PHX activates fusion and/or maturation of endosomes. Formaldehyde-treated bovine serum albumin is known to be taken up by the liver by receptor-mediated endocytosis. The uptake of the modified heterologous albumin was shown to be activated Astelin Buy as early as 30 min after PHX. Both the uptake of serum albumin into lysosomes and the shift of buoyant density profile of endosomes after PHX were inhibited by the administration of adrenergic receptor antagonists, particularly by the alpha r-antagonist prazosin. Further, the concentration of catecholamines in rat serum, particularly that of norepinephrine, was found to increase immediately after PHX, relative to that in serum from sham-operated rats. These results suggest that the elevation of serum norepinephrine levels after PHX activates endocytosis and facilitates delivery of endocytosed serum albumin to lysosomes, where albumin is digested to yield amino acids for possible use in protein synthesis during liver regeneration.

minipress overdose death 2015-12-25

The purpose of this study was to examine the influence of ageing on the alterations in binding characteristics of adrenoceptors and membrane phospholipid fatty acids in rat heart following repeated administration of epinephrine. The maximal number of binding sites (Bmax) and dissociation constant (Kd) of [3H]prazosin and [3H]dihydroalprenolol binding to alpha 1- and beta-adrenoceptors, respectively, changed significantly during ageing. The downregulation of alpha 1- and beta-adrenoceptors after repeated epinephrine administration for one week, did not differ with age, but the response of the affinity (1/Kd) of both alpha 1- and beta-adrenoceptors to epinephrine treatment was age dependent. In 3-month-old rats the affinity of alpha 1-adrenoceptors was decreased after epinephrine treatment but the affinity of beta-adrenoceptors was unchanged. In 10- and 23-month-old rats the affinity of beta-adrenoceptors decreased after epinephrine treatment but the affinity of alpha 1-adrenoceptors did not change. During ageing the linoleic acid (18:2(n-6)) level decreased in phosphatidylcholine and the arachidonic acid (20:4(n-6)) level increased in phosphatidylcholine and phosphatidylethanolamine. After epinephrine administration the 18:2(n-6) level decreased and the docosahexaenoic acid (22:6(n-3)) level Clomid 4 Pills increased in phosphatidylcholine and phosphatidylethanolamine and those changes were not age dependent. The 20:4(n-6) level increased in phosphatidylcholine after epinephrine administration, but that increase was smaller in old than in young rats. The results show that both ageing and epinephrine administration simultaneously modify the fatty acid composition of membrane phospholipids and the binding properties of alpha 1- and beta-adrenoceptors in rat heart.

minipress max dose 2015-08-02

The chick pineal gland expresses a circadian rhythm of melatonin biosynthesis, with elevated levels at night and low levels during the day. The rhythm of melatonin is regulated both by circadian oscillators located within the gland itself and by adrenergic input from the sympathetic nervous system. Previous work has shown that norepinephrine administration inhibits melatonin biosynthesis, as measured by the activity of the enzyme serotonin N-acetyltransferase. As a first step toward understanding the mechanisms by which norepinephrine regulates melatonin production in the chick pineal, we have identified the adrenergic receptor involved. Dissociated chick pineal cell cultures were prepared and melatonin release was measured on days 5 and 6 of culture using radioimmunoassay. The effects of adrenergic agonists and antagonists on the nocturnal increase of melatonin release during the 12 Zantac 300mg Dosage hr dark portion of a LD12:12 light cycle were determined. Norepinephrine inhibited melatonin release in a dose-dependent manner, with an average EC50 of 19.7 nM +/- 2.23 (SEM). Melatonin release values ranged from 100 to 4% of the level seen in control cultures, depending on the dose of norepinephrine. The physiological response to epinephrine, norepinephrine, and isoproterenol was stereospecific. The (-) stereoisomer was 6, 8, and 37 times more potent than the (+) stereoisomer, respectively. EC50 values (in nM) for adrenergic agonists were as follows: alpha-methyl-(-)-norepinephrine, 2.46; tramazoline, 3.06; guanabenz, 3.31; clonidine, 3.70; oxymetazoline, 4.29; (-)-epinephrine, 7.44; (-)-norepinephrine, 19.7; (-)-isoproterenol, 463; and (-)-phenylephrine, 659. Schild analysis was used to determine the relative potency of adrenergic antagonists. pA2 values for adrenergic antagonists were as follows: rauwolscine, 9.55; RX78 1094, 8.32; yohimbine, 8.14; phentolamine, 7.11; prazosin, 5.93; and (-)-propranolol, less than 6. The relative potencies of both adrenergic agonists and antagonists demonstrate that alpha-2 receptors mediate norepinephrine-induced inhibition of melatonin release in chick pineal cell cultures. The identification of alpha-2 receptors in chick pineal cells should aid in our understanding of the biochemical events initiated by receptor activation that regulate melatonin synthesis.

minipress generic name 2016-12-15

In heart failure, homologous downregulation of beta-adrenoceptors contributes to impaired adrenergic responsiveness of the myocardium. We Avodart Drug evaluated alpha 1-adrenoceptors (alpha 1-AR) in a sparsely innervated and a densely innervated peripheral artery in an experimental model of left ventricular dysfunction post-myocardial infarction.

minipress 6 mg 2015-09-02

1. The antinociceptive action of clonidine (Clon) and the interactions with alpha 1, alpha 2 adrenoceptor and opioid receptor antagonists was evaluated in mice by use of chemical algesiometric test (acetic acid writhing test). 2. Clon produced a dose-dependent antinociceptive action and the ED50 for intracerebroventricular (i.c.v.) was lower than for intraperitoneal (i.p.) administration (1 ng kg-1 vs 300 ng kg-1). The parallelism of the dose-response curves indicates activation of a common receptor subtype. 3. Systemic administration of prazosin and terazosin displayed antinociceptive activity. Pretreatment with prazosin produced a dual action: i.c.v. Clon effect did not change, and i.p. Clon effect was enhanced. Yohimbine i.c.v. or i.p. did not induce antinonciception, but antagonized Clon-induced activity. These results suggest that alpha 1- and alpha 2-adrenoceptors, either located at the pre- and/or post-synaptic level, are involved in the control of spinal antinociception. 4. Naloxone (NX) and naltrexone (NTX) induced antinociceptive effects at low doses (microgram kg-1 range) and a lower antinociceptive effect at higher doses (mg kg-1 range). Low doses of NX or NTX antagonized Clon antinociception, possibly Accutane Online Pharmacy in relation to a preferential mu opioid receptor antagonism. In contrast, high doses of NX or NTX increased the antinociceptive activity of Clon, which could be due to an enhanced inhibition of the release of substance P. 5. The results obtained in the present work suggest the involvement of alpha 1-, alpha 2-adrenoceptor and opioid receptors in the modulation of the antinociceptive activity of clonidine, which seems to be exerted either at spinal and/or supraspinal level.

minipress medication information 2017-01-25

Both kinetic and equilibrium data support Cleocin Alcohol the presence of at least two symmetric drug binding sites on ABCG2, which is distinct from the asymmetry observed for P-gp. The data provide the first molecular details underlying the mechanism by which this transporter is capable of interacting with multiple substrates.