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Adalat (Nifedipine)

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Adalat is a high-quality medication which is taken in treatment of hypertension or high blood pressure, angina or chest pain. Adalat acts by relaxing blood vessels (such as veins and arteries), which makes it easier for the heart to pump and reduces its workload.

Other names for this medication:

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Also known as:  Nifedipine.


Adalat is a perfect remedy in struggle against hypertension or high blood pressure, angina or chest pain.

Adalat acts by relaxing blood vessels (such as veins and arteries), which makes it easier for the heart to pump and reduces its workload.

Adalat is also known as Nifedipine, Nicardia, Nifedical, Procardia.

Generic name of Adalat is Nifedipine.

Brand names of Adalat are Adalat CC, Procardia, Procardia XL.


Adalat should be taken orally with or without food.

It is better to take Adalat at the same time every day. Take on an empty stomach.

Avoid grapefruit juice during treatment with Adalat.

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


If you overdose Adalat and you don't feel good you should visit your doctor or health care provider immediately.


Store at room temperature between 15 and 25 degrees C (59 and 77 degrees F) away from moisture and heat. Keep container tightly closed. Throw away any unused medicine after the expiration date. Keep out of the reach of children.

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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.


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

Do not take Adalat if you're pregnant or you plan to have a baby, or you are a nursing mother. Adalat can harm your baby.

Do not use Adalat in combination with salt substitutes or potassium supplements.

If you want to achieve most effective results without any side effects it is better to avoid alcohol.

Avoid grapefruit juice during treatment with Adalat.

Try to be careful using Adalat if you suffer from kidney disease, liver disease, diseases of the heart or blood vessels (sick sinus syndrome), aortic stenosis, heart failure, low blood pressure, or coronary artery disease.

Do not stop taking Adalat suddenly.

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In rats with renovascular hypertension and hypertensive heart disease that included LVH and fibrosis, equipotent doses of ZOF, NIF, and LAB normalized arterial pressure associated with regression of LVH while only ZOF and NIF were found to regress myocardial fibrosis.

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Hypothalamic AMP-activated protein kinase (AMPK) and orexins/hypocretins are both involved in the control of feeding behavior, but little is known about the interaction between these two signaling systems. Here, we demonstrated that orexin-A elicited significant activation of AMPK in the arcuate nucleus (ARC) of the hypothalamus by elevating cytosolic free Ca²⁺ involving extracellular calcium influx. Electrophysiological results revealed that orexin-A increased the L-type calcium current via the orexin receptor-phospholipase C-protein kinase C signaling pathway in ARC neurons that produce neuropeptide Y, an important downstream effector of orexin-A's orexigenic effect. Furthermore, the L-type calcium channel inhibitor nifedipine attenuated orexin-A-induced AMPK activation in vitro and in vivo. We found that inhibition of AMPK by either compound C (6-[4-[2-(1-piperidinyl)ethoxy]phenyl]-3-(4-pyridinyl)-pyrazolo[1,5-a]pyrimidine) or the ATP-mimetic 9-β-D-arabinofuranoside prevented the appetite-stimulating effect of orexin-A. This action can be mimicked by nifedipine, the blocker of the L-type calcium channel. Our results indicated that orexin-A activates hypothalamic AMPK signaling through a Ca²⁺-dependent mechanism involving the voltage-gated L-type calcium channel, which may serve as a potential target for regulating feeding behavior.

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The paediatric ERF population continued to expand slowly. Incidence and prevalence rates were stable and similar to other developed nations. The high incidence in patients from ethnic minority groups will lead to a greater proportion of the population being from these groups in time. To maintain the high proportion of engrafted patients it will be necessary to encourage living donation in the ethnic minority population. The spectrum of diseases seen has already changed over a generation with the treatment of young children with diseases such as congenital nephrosis. The incidence of cystinosis causing ERF was reduced, probably reflecting better early treatment.

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The effect of betulinic acid, an anti-tumor and apoptosis-inducing natural product, on intracellular-free levels of Ca(2+) ([Ca(2+)](i)) in Madin Darby canine kidney (MDCK) cells was examined by using fura-2 as a Ca(2+) dye. Betulinic acid caused significant increases in [Ca(2+)](i) concentration dependently between 25 and 500 nM with an EC(50) of 100 nM. The [Ca(2+)](i) signal was composed of an initial gradual rise and a plateau. The response was decreased by removal of extracellular Ca(2+) by 45+/-10%. In Ca(2+)-free medium, pretreatment with 1 microM thapsigargin (an endoplasmic reticulum Ca(2+) pump inhibitor) abolished 250 microM betulinic acid-induced [Ca(2+)](i) increases. Conversely, pretreatment with betulinic acid only partly inhibited thapsigargin-induced [Ca(2+)](i) increases. Addition of 3 mM Ca(2+) induced a [Ca(2+)](i) increase after pretreatment with 250 nM betulinic acid in Ca(2+)-free medium for 5 min. This [Ca(2+)](i) increase was not altered by the addition of 20 microM SKF96365 and 10 microM econazole. Inhibiting inositol 1,4,5-trisphosphate formation with the phospholipase C inhibitor U73122 (2 microM) abolished 250 nM betulinic acid-induced Ca(2+) release. Pretreatment with 10 microM La(3+) inhibited 250 nM betulinic acid-induced [Ca(2+)](i) increases by 85+/-3%; whereas 10 microM of verapamil, nifedipine and diltiazem had no effect. In Ca(2+) medium, pretreatment with 2.5 nM betulinic aid for 260 s potentiated 10 microM ATP and 1 microM thapsigargin-induced [Ca(2+)](i) increases by 33+/-3% and 45+/-3%, respectively. Trypan blue exclusion revealed that acute exposure of 250 nM betulinic acid for 2-30 min decreased cell viability by 6+/-2%, which could be prevented by pretreatment with 2 microM U731222. Together, the results suggest that betulinic acid induced significant [Ca(2+)](i) increases in MDCK cells in a concentration-dependent manner, and also induced mild cell death. The [Ca(2+)](i) signal was contributed by an inositol 1,4, 5-trisphosphate-dependent release of intracellular Ca(2+) from thapsigargin-sensitive stores, and by inducing Ca(2+) entry from extracellular medium in a La(3+)-sensitive manner.

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We previously reported that a calcium channel blocker supplemented immunosuppression produced excellent patient and graft survival rates in cadaveric kidney transplantation. We report here the long term outcome of patients treated with nifedipine-supplemented triple immunosuppression as compared with those of historical controls who were treated similarly without nifedipine. Study subjects included 111 patients transplanted in 1990-1994, treated with nifedipine and triple immunosuppression and with functioning grafts for more than one year (Nifedipine group). The results of cyclosporine (CyA) dose, blood pressure (BP), serum creatinine (Cr), and actuarial graft survival rate (GSR) up to 5 years posttransplant in these patients were compared with those of 52 patients transplanted in 1985-1990, treated similarly without calcium channel blockers (Control group). Donor sources, gender ratio, age distribution, causes of end stage renal disease, incidence of hypertension prior to transplantation and incidence of rejection in the first year between the groups were comparable. Throughout the study period the Nifedipine group had significantly lower serum Cr (1.5 +/- 0.7 vs. 1.8 +/- 0.7 mg/dl) and higher GSR (93.8% vs. 88% at 5 years) than the Control group. BP was comparable despite higher CyA doses in the Nifedipine group (4.3 +/- 1.1 vs. 3.3 +/- 1.1 mg/kg/day). We conclude that nifedipine is beneficial in improving long-term graft function and survival in kidney transplant recipients by mitigating CyA associated renal injury.

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A total of 400 patients met the inclusion criteria; out of the 400 patients studied, 63.5% were females. Most of the patients had Stage 1 hypertension (69%), followed by Stage 2 hypertension (31%). Out of the total number of patients, 264 were with different comorbid conditions: diabetes mellitus (64.3%), followed by congestive heart failure (15.1%) and ischemic heart disease (2.3%). The most frequently prescribed class of antihypertensive drugs was diuretics, of which hydrochlorothiazide was the most frequently prescribed drug, both in single (55%), followed by enalapril (22.3%), methyl dopa (11.2%), atenolol (6.9%), and nifedipine (4.6%), and in combination with other antihypertensive drugs. The average dispensing time was 1.2 minutes, and 75% of the patients left the counter with inadequate information about the dosage.

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After infusion, blood flow, digitally measured by telethermography was increased only in patients treated with alprostadil. The number, frequency and severity of attacks recorded were reduced only in patients treated with alprostadil. No side effects were recorded during and after the infusion.

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1. The pharmacological and kinetic properties of two types of low-voltage-activated (LVA) Ca2+ currents were studied in thalamocortical neurones of the laterodorsal (LD) thalamic nucleus during early postnatal development. The whole-cell patch-clamp technique was used on brain slices from rats of three age groups: 12, 14 and 17 days old (postnatal day (P) 12, P14 and P17). 2. In P12 neurones, the population of LVA Ca2+ channels was homogeneous. LVA Ca2+ current elicited by depolarizing voltage steps from a holding potential more negative than -70 mV was sensitive to nifedipine (Kd = 2.6 microM). This current reached a maximum at about -55 mV and had a fast monoexponential decay with a time constant, tau h,f, of 32.3 +/- 4.0 ms. 3. The population of LVA Ca2+ channels in P14 and P17 neurones was found to be heterogeneous. A subpopulation of nifedipine-insensitive LVA Ca2+ channels was observed. The current-voltage curve of the Ca2+ current had a characteristic hump with two peaks at about -65 and -55 mV. As well as the fast component (designated IT,f), the decay of the LVA current also included a slow component (designated IT,s), with inactivation time constants (tau h,s) of 54.2 +/- 4.5 and 68.6 +/- 3.17 ms for P14 and P17 neurones, respectively. 4. The kinetics of both components could be well approximated by the m2h Hodgkin-Huxley equation. No significant difference in activation kinetics was observed. The activation time constants for the fast (tau m,f) and slow (tau m,s) components were 6.3 +/- 1.0 and 7.3 +/- 1.5 ms, respectively. 5. La3+ at a concentration of 1 microM effectively blocked the IT,f component but Ni2+ (25 microM) completely eliminated the IT,s component. 6. Steady-state inactivation curves of both components could be best fitted by a Boltzmann function with membrane potential values at half-maximal inactivation of -85.5 and -98.1 mV for the fast and slow components, respectively. 7. It was concluded that two different subtypes of LVA Ca2+ channel are present in LD neurones. Only the fast type is well expressed at the earliest postnatal stage (P12). The slow type could be found at the end of the second week (P14). The amplitude of the slow current increased progressively up to P17, obviously coinciding with dendritic expansion as judged by progressive increase of the membrane capacitance of the corresponding neurones. This property appears to differentiate neurones of the associative nuclei from neurones of other thalamic nuclei.

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Oxaliplatin (4 mg/kg) induced cold hyperalgesia and increased in the transient receptor potential melastatin 8 (TRPM8) mRNA levels in the dorsal root ganglia (DRG). Furthermore, oxalate (1.3 mg/kg) significantly induced the increase in TRPM8 protein in the DRG. Treatment with oxaliplatin and oxalate (500 μM for each) also increased the TRPM8 mRNA levels and induced Ca²⁺ influx and nuclear factor of activated T-cell (NFAT) nuclear translocation in cultured DRG cells. These changes induced by oxalate were inhibited by nifedipine, diltiazem and mexiletine. Interestingly, co-administration with nifedipine, diltiazem or mexiletine prevented the oxaliplatin-induced cold hyperalgesia and increase in the TRPM8 mRNA levels in the DRG.

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It was concluded that gingival enlargement occurs in patients with nifedipine therapy only in the areas where local inflammatory factors are present.

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The objective of this study was to prepare spontaneous emulsifying powder (SEP) for improving dissolution and enhancing oral bioavailability of a poorly water-soluble drug, nifedipine (NDP). In order to investigate the effects of solid carrier properties, such as surface area and pore size, and a concurrent food intake on absorption of NDP in rats, different SEP formulations were prepared by adsorbing liquid spontaneous emulsifying formulation (SEF), composing of polyoxyl 35 castor oil, caprylic/capric glyceride and diethylene glycol monoethyl ether at a ratio of 1:1:8, onto various solid carriers (i.e., silica (FS), porous calcium silicate (PCS) and porous silicon dioxide). The solid characterization by scanning electron microscopy, differential scanning calorimetry and powder X-ray diffraction revealed the absence of crystalline NDP in the formulations. SEP also demonstrated excellent spontaneous emulsification properties similar to SEF. The droplet size of emulsions formed after dilution was less than 200 nm. The solid carriers (particularly PCS) had significant and positive effect in drug dissolution; the mean dissolution time of SEP containing PCS was considerably improved. SEP also provided a good stability after storage in accelerated and long-term conditions for 6 months. The bioavailability study resulted in enhanced values of C(max) and AUC for SEP formulations, when tested in both fasted and fed rats. Furthermore, comparing the AUC in fasted and fed rats, NDP powder exhibited a significant food effect. The difference in bioavailability of NDP in fed compared to fasted state can be avoided by using SEP.

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Natural halloysite clay nanotubes with 15 nm inner and 75 nm outer diameters have been used as vehicles for sustained release of drugs in composite hollow microparticles "glued" with CaCO3. We used a layer-by layer assembly accomplished alginate binding with Ca(2+) followed by CO2 bubbling to prepare the composite microspheres of CaCO3 and polyelectrolytes (PE) modified halloysite nanotubes (HNTs-PE2/CaCO3) with the diameter of about 5-10 μm. These microparticles have empty spherical structure and abundant pore distributions with maxima at 2.5, 3.9, 6.0 and 13.3 nm, and higher surface area of 82.3 m(2) g(-1) as characterized by SEM and BET test. We loaded drugs in these micro-nano carriers of tight piles of halloysite nanotube with end clogged with CaCO3. The sustained release of Nifedipine drug from HNTs-PE2/CaCO3 composite microspheres was slower than for pristine halloysite nanotubes.

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The treatment of systemic sclerosis (scleroderma) is difficult and remains a great challenge to the clinician. Because the cause is unknown, therapies are directed to improve peripheral blood circulation with vasodilators and antiplatelet aggregation drugs, to prevent the synthesis and release of harmful cytokines with immunosuppressant drugs, and to inhibit or reduce fibrosis with agents that reduce collagen synthesis or enhance collagenase production. The purpose of this review is to critically analyze conventional and new treatments of systemic sclerosis and localized scleroderma. The therapeutic options discussed for the treatment of systemic sclerosis include the use of (1) vasodilators (calcium channel blockers [nifedipine], angiotensin-converting enzyme inhibitors [captopril, losartan potassium], and prostaglandins [iloprost, epoprostenol]), (2) immunosuppressant drugs (methotrexate, cyclosporine, cyclophosphamide, and extracorporeal photopheresis), and (3) antifibrotic agents (D-penicillamine, colchicine, interferon gamma, and relaxin). The treatment options reviewed for localized scleroderma include the use of corticosteroids, vitamin D analogues (calcitriol, calcipotriene), UV-A, and methotrexate. Preliminary reports on new therapies for systemic sclerosis are also considered. These include the use of minocycline, psoralen-UV-A, lung transplantation, autologous stem cell transplantation, etanercept, and thalidomide.

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Plasticity at the neuronal level commonly involves use-dependent changes in strength of particular synaptic pathways or regulation of postsynaptic properties by modulatory transmitters. Here we analyze a novel form of short-term plasticity mediated by use-dependent facilitation of postsynaptic responsiveness. Using current- and voltage-clamp recordings, we found that all spinal ventral horn neurons able to generate plateau potentials showed depolarization-induced facilitation of the underlying inward current. Facilitation was noticeable when the neurons were depolarized to more than -50 mV at intervals <4 s. When stimulation with fast triangular voltage ramps was used, the inward current activated at a less depolarized potential during the second ramp. The inward current and facilitation was eliminated by nifedipine, a selective antagonist of L-type calcium channels. Depolarization-induced facilitation of low-voltage-activated L-type calcium channels is suggested to be the underlying mechanism. It is noted that facilitation occurs on a time scale compatible with a role in phasic motor activity.

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The aims of this review paper are: (1) to identify the pharmacological basis of interference of a variety of substances with MIBG uptake; and (2) to update the list of drugs that definitely interfere with MIBG on the grounds of evidence in the literature.

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Aging creates deficits in motor performance related to changes in striatal processing of cortical information. This study describes age-related changes in corticostriatal snaptic plasticity and associated mechanisms, which may contribute to declines in motor behavior. Intracellular recordings revealed an age-related decrease in the expression of paired-pulse, posttetanic, and long-term potentiation (LTP). The age-related difference in LTP was associated with reduced sensitivity to block of N-methyl-D-aspartate (NMDA) receptors in the aged population. These age-related changes could not be explained by increased L-type Ca(2+)channel activity, since block of L-type Ca(2+) channels with nifedipine increased rather than decreased the age-related difference in long-term plasticity. Age-related increases in reactive oxygen species (ROS) modulation were also ruled out, since application of H(2)O(2) produced changes in synaptic function that were opposite to trends seen in aging, and addition of the antioxidant Trolox-C had a larger effect on long-term plasticity in young rats than in older rats. A robust age-related difference in long-term synaptic plasticity was found by studying synaptic plasticity following the blocking of D2 receptors with l-sulpiride, which may involve age-difference in NMDA receptor function. l-sulpiride consistently enabled a slow development of LTP at young (but not aged) corticostriatal synapses. However, No age differences were found in the sensitivity to the addition of the D2 receptor agonist quinpirole. These findings provide evidence for age-induced changes in the release properties of cortical terminals and in the functioning of postsynaptic striatal NMDA receptors, which may contribute to age-related deficits in striatum control of movement.

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BACKGROUND: In the intact immature heart, how much digoxin can drive sodium-calcium exchange has not been studied in the context of sodium-calcium exchanger abundance. METHODS AND RESULTS: The effects of digoxin and low potassium on contractility in the intact, paced and isovolumically contracting immature rabbit heart were studied in both the absence and presence of L-type calcium channel blockade. Without calcium channel blockade, digoxin increased contractility minimally and only at 10(_6) M/L. In contrast, low potassium (2.2 mM/L) substantially increased contractility in all experiments, a result indicating abundant sodium-calcium exchanger activity. During nifedipine-induced calcium channel blockade, digoxin (10(_6) M/L) allowed modest recovery of contractility, whereas digoxin and low potassium together allowed complete recovery as assessed by dP/dt(max); however, all hearts so perfused subsequently developed ventricular fibrillation, presumably because of calcium overload. CONCLUSIONS: In intact immature rabbit heart, digoxin can drive sodium-calcium exchange and thus increase contractility to only a minimal extent. This effect does not appear to be limited by intrinsic exchanger activity, which appears abundant in this preparation. Rather, digoxin's inability to drive the sodium-calcium exchanger may be due to developmental differences in binding to the sodium pump. The sodium-calcium exchanger itself seems capable not only of providing enough intracellular calcium for normal contraction, but also of overloading the myocardium with calcium, despite L-type calcium channel blockade.

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The superior colliculus in mammals or the optic tectum in amphibians is a major visual information processing center responsible for generation of orientating responses such as saccades in monkeys or prey catching avoidance behavior in frogs. The conserved structure function of the superior colliculus the optic tectum across distant species such as frogs, birds monkeys permits to draw rather general conclusions after studying a single species. We chose the frog optic tectum because we are able to perform whole-cell voltage-clamp recordings fluorescence imaging of tectal neurons while they respond to a visual stimulus. In the optic tectum of amphibians most visual information is processed by pear-shaped neurons possessing long dendritic branches, which receive the majority of synapses originating from the retinal ganglion cells. Since the first step of the retinal input integration is performed on these dendrites, it is important to know whether this integration is enhanced by active dendritic properties. We demonstrate that rapid calcium transients coinciding with the visual stimulus evoked action potentials in the somatic recordings can be readily detected up to the fine branches of these dendrites. These transients were blocked by calcium channel blockers nifedipine CdCl2 indicating that calcium entered dendrites via voltage-activated L-type calcium channels. The high speed of calcium transient propagation, >300 μm in <10 ms, is consistent with the notion that action potentials, actively propagating along dendrites, open voltage-gated L-type calcium channels causing rapid calcium concentration transients in the dendrites. We conclude that such activation by somatic action potentials of the dendritic voltage gated calcium channels in the close vicinity to the synapses formed by axons of the retinal ganglion cells may facilitate visual information processing in the principal neurons of the frog optic tectum.

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The Medline databank was used to search studies in human beings (published in 1990 or later) that used dihydropyridines in patients with CHF. The references of the studies found were subsequently checked for additional data. In 17 studies and more than 2000 patients with CHF, no consistent beneficial effect was observed with regard to exercise tolerance and functional capacity, whereas plasma neurohormones were not affected. On the other hand, in general, no worsening of CHF was seen with these second-generation dihydropyridines. Two larger studies (PRAISE and V-HeFT III) have given some estimates on the long-term effects of dihydropyridines, and no overall influence on mortality rate was found. Of note, subanalysis of the PRAISE study has suggested that in patients with a nonischemic cause of CHF, amlodipine might have a beneficial effect on survival.

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Changes in intracellular Na+ and Ca2+ in inspiratory neurons of neonatal mice were examined by using ion-selective fluorescent indicator dyes SBFI and fura-2, respectively. Both [Na+]i and [Ca2+]i signals showed rhythmic elevations, correlating with the inspiratory motor output. Brief (2-3 min) hypoxia, induced initial potentiation of rhythmic transients followed by their depression. During hypoxia, the basal [Na+]i and [Ca2+]i levels slowly increased, reflecting development of an inward current (Im). By antagonizing specific mechanisms of Na+ and Ca2+ transport we found that increases in [Na+]i, [Ca2+]i and Im due to hypoxia are suppressed by CNQX, nifedipine, riluzole and flufenamic acid, indicating contribution of AMPA/kainate receptors, persistent Na+ channels, L-type Ca2+ channels and Ca2+-sensitive non-selective cationic channels, respectively. The blockers decreased also the amplitude of the inspiratory bursts. Modification of mitochondrial properties with FCCP and cyclosporine A decreased [Ca2+]i elevations due to hypoxia by about 25%. After depletion of internal Ca2+ stores with thapsigargin, the blockade of NMDA receptors, Na+/K+ pump, Na+/H+ and Na+/Ca2+ exchange, the hypoxic response was not changed. We conclude that slow [Na+]i and [Ca2+]i increases in inspiratory neurons during hypoxia are caused by Na+ and Ca2+ entry due to combined activation of persistent Na+ and L-type Ca2+ channels and AMPA/kainate receptors.

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Preglomerular VSMCs have functional RyR, and a capacitative (store-operated) entry mechanism is activated by the depletion of SR Ca2+ with ryanodine, as is the case with inhibitors of SR Ca2+-ATPase.

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Both H(2)O(2) and ATP induced transient phasic contractions in a concentration-dependent manner (1-1000 microM). Removal of endothelium potentiated the contractile responses to H(2)O(2) and to ATP. H(2)O(2) (30 microM)-induced phasic contraction could be abolished by catalase (800 U/ml), but not affected by SOD (150 U/ml), DMSO (5 mM) and apyrase (5 U/ml), suggesting no involvement of O(2)(-), hydroxyl free radicals and ATP release. Also, several receptor antagonists including phentolamine, atropine, methysergide and chlorpheniramine (each 3 microM) were without effect on H(2)O(2) (30 microM)-induced phasic contraction, suggesting no involvement of typical neurotransmitter release. However, both H(2)O(2) (30 microM) and ATP (1 mM)-induced phasic contractions not only presented homologous desensitization, but also showed heterogeneous desensitization. Furthermore, the phasic contractions in response to H(2)O(2) (30 microM) or ATP (100 microM) could be inhibited or abolished in a concentration dependent manner by RB-2 and suramin (10-100 microM), two widely used P(2)-purinoceptor antagonists, with only partial inhibition by Evans blue (300 microM), a moderately selective P(2x) receptor blocker, or by alpha-beta-methylene-ATP (100 microM), a selective P(2x) receptor desensitizer. On the other hand, both H(2)O(2) (30 microM) and ATP (100 microM)-induced phasic contractions were also attenuated, to different degree, by inhibitors of several enzymes including PLC, PKC, PLA(2) and cyclooxygenase. Lastly, removal of extracellular Ca(2+) or pretreatment with procaine (10 mM) and dantrolene (30 microM), two putative intracellular Ca(2+) release blockers, or with Ni(2+) (100 microM) and tetrandrine (5 microM), two Ca(2+) channel blockers, all significantly inhibited H(2)O(2) and ATP-induced contractions. However, nifedipine (1 microM), a voltage-dependent L-type Ca(2+) channel blocker, was without effect.

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The aims of this study were to determine whether systemic injections of the lipophobic thiol chelator, para-hydroxymercurobenzoic acid (PHMBA) would reduce the vasoconstrictor responses elicited by the alpha1-adrenoceptor agonist, phenylephrine, in urethane-anesthetized rats by chelation of thiol residues in alpha1-adrenoceptors in vascular smooth muscle rather than voltage-sensitive Ca(2+)-channels (Ca(2+)VERSUS-channels). The magnitudes and durations of the vasoconstrictor responses elicited by phenylephrine were markedly reduced after the injections of PHMBA. In contrast, the maximal phenylephrine-induced responses were not affected whereas the durations of these responses were markedly attenuated after injection of the Ca(2+)VERSUS-channel blocker, nifedipine. Nifedipine elicited pronounced and sustained falls in mean arterial blood pressure and vascular resistances in PHMBA-treated rats. Moreover, the vasodilator actions of the nitric oxide-donor, sodium nitroprusside were minimally attenuated by PHMBA whereas they were markedly attenuated by nifedipine. These findings support evidence that the vasoconstrictor responses due to activation of alpha1-adrenoceptors are initiated by mobilization of intracellular pools of Ca(2+) whereas they are sustained by opening of Ca(2+)VERSUS-channels. These findings also suggest that PHMBA diminishes the vasoconstrictor effects of phenylephrine by chelation of thiol residues in alpha1-adrenoceptors rather than by blockade of Ca(2+)VERSUS-channels, and that chelation of these thiol residues prevents agonist occupation and/or activation of these receptors and subsequent mobilization of intracellular pools of Ca(2+).

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adalat xl dose 2015-01-25

Eighteen patients, 11 men and seven women with a median age of 61.7 years, were imaged before and 6 weeks after the initiation of 30 mg of sustained-release nifedipine (Procardia XL; produced by either Pfizer or Pratt) buy adalat daily.

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Apamin-sensitive small conductance Ca(2+)-dependent K(+)(SK) channels are generally accepted as responsible for the medium afterhyperpolarization (mAHP) after single or train of action potentials. Here, we examined buy adalat the functional involvement of these channels in the firing precision, post train AHP and spike frequency adaptation (SFA) in neurons of snail Caucasotachea atrolabiata. Apamin, a selective SK channel antagonist, reduced the duration of single-spike AHP and disrupted the spontaneous rhythmic activity. High frequency trains of evoked action potentials showed a time-dependent decrease in the action potential discharge rate (spike frequency adaptation) and followed by a prominent post stimulus inhibitory period (PSIP) as a marker of slow AHP (sAHP). Neither sAHP nor SFA was attenuated by apamin, suggesting that apamin-sensitive SK channels can strongly affect the rhythmicity, but are probably not involved in the SFA and sAHP. Nifedipine, antagonist of L-type Ca(2+) channels, decreased the firing frequency and neuronal rhythmicity. When PSIP was normalized to the background interspike interval, a suppressing effect of nifedipine on PSIP was also observed. Intracellular iontophoretic injection of BAPTA, a potent Ca(2+) chelator, dramatically suppressed PSIP that confirms the intracellular Ca(2+) dependence of the sAHP, but had no discernable effect on the SFA. During train-evoked activity a reduction in the action potential overshoot and maximum depolarization rate was also observed, along with a decrease in the firing frequency, while the action potential threshold increased, which indicated that Na(+) channels, rather than Ca(2+)-dependent K(+) channels, are involved in the SFA.

adalat 50 mg 2017-08-10

Several clinical cases of severe bradyarrhythmias have been reported upon co-administration of the Hepatitis-C NS5B Nucleotide Polymerase Inhibitor (HCV-NI) direct-acting antiviral agent, sofosbuvir (SOF), and the Class-III anti-arrhythmic amiodarone (AMIO). We model the cardiac drug-drug interaction (DDI) between AMIO and SOF, and between AMIO and a closely-related SOF analog, MNI-1 (Merck Nucleotide Inhibitor #1), in functional assays of human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs), to provide mechanistic insights into recently reported clinical cases. AMIO co-applied with SOF or MNI-1 increased beating buy adalat rate or field potential (FP) rate and decreased impedance (IMP) and Ca(2+) transient amplitudes in hiPSC-CM syncytia. This action resembled that of Ca(2+) channel blockers (CCBs) in the model, but CCBs did not substitute for AMIO in the DDI. AMIO analog dronedarone (DRON) did not substitute for, but competed with AMIO in the DDI. Ryanodine and thapsigargin, decreasing intracellular Ca(2+) stores, and SEA-0400, a Na(+)/Ca(2+) exchanger-1 (NCX1) inhibitor, partially antagonized or suppressed DDI effects. Other agents affecting FP rate only exerted additive or subtractive effects, commensurate with their individual effects. We also describe an interaction between AMIO and MNI-1 on Cav1.2 ion channels in an over-expressing HEK-293 cell line. MNI-1 enhanced Cav1.2 channel inhibition by AMIO, but did not affect inhibition of Cav1.2 by DRON, verapamil, nifedipine, or diltiazem. Our data in hiPSC-CMs indicate that HCV-NI agents such as SOF and MNI-1 interact with key intracellular Ca(2+)-handling mechanisms. Additional study in a Cav1.2 HEK-293 cell-line suggests that HCV-NIs potentiate the inhibitory action of AMIO on L-type Ca(2+) channels.

adalat cc generic 2015-03-08

The use of montelukast modified the capillary abnormalities observed on nailfold capillaroscopy of patients with Raynaud buy adalat 's phenomenon.

adalat 40 mg 2015-12-14

The randomised controlled trials included in this review provide moderate quality evidence that oral calcium channel blockers are minimally effective in the treatment of primary Raynaud's phenomenon as measured by the frequency of attacks and high-quality evidence that they have little effect on severity. We are unable to comment on duration of attacks or on patient preference due to the very low and low quality of evidence as a buy adalat result of small sample sizes in the included studies and the variable data quality of outcome measures.

adalat xl dosing 2015-01-17

Morphine and methadone share the property of μ-opioid receptor agonism yet have markedly different cardiovascular actions suggesting additional properties are at play. We investigated the i.v. dose-response relationships of the opioids on cardiovascular metameters in anaesthetised rats in the absence or presence of H1- and H2-receptor antagonism and the μ-opioid antagonist naloxone. In vitro tissue assays were employed to define more clearly cardiac and vascular mechanisms of action. Morphine (9, 30, 90mg/kg i.v.) decreased heart rate (HR) and mean arterial pressure (MAP) - responses that were blocked by naloxone pretreatment (10mg/kg i.v.). In contrast, methadone (3, 10, 30mg/kg i.v.) caused dramatic short-lived (1-3min) bradycardia, hypotension and lengthening of the QT interval before stabilising 5min after i.v. dosing. Only the steady-state responses of HR and MAP were blocked by naloxone. Mepyramine (10mg/kg i.v.) and cimetidine (100mg/kg i.v.) also blocked the naloxone-sensitive components. In isolated small mesenteric arteries precontracted by K(+) 62mM or endothelin-1, methadone (1-30μM) relaxed vessels while morphine (1-100μM) had no effect. Pretreatment with naloxone (10μM), indomethacin (30μM) or nitro-l buy adalat -arginine (100μM) did not affect the relaxation to methadone. In rat isolated left atria, morphine and methadone inhibited inotropic responses at high concentrations (100μM). In rat papillary muscle and right atria, methadone was more than 30 times more potent at lengthening the refractory period and slowing the atrial rate than morphine. We conclude that methadone is a potent vasodilator agent, possibly through blocking L-type calcium channels.

adalat cc dosage 2016-03-06

A MEDLINE search (January 1966-December 1997) of the English-language literature pertaining to bezoars was performed. These articles were scanned, and literature specifically discussing medication bezoars was selected. Additionally, the reference buy adalat sections of pertinent review and case reports were scanned for additional relevant literature.

adalat r dose 2015-02-08

Large systemic doses of morphine administered to some patients for cancer pain management have been reported to produce myoclonus and allodynia. Indirect evidence implicates the major morphine metabolite, morphine-3-glucuronide (M3G), in these neuro-excitatory side effects. Hence, this study was designed buy adalat to gain insight into the cellular mechanism responsible for M3G's neuro-excitatory actions.

adalat generic name 2016-06-17

Calcium buy adalat channel blockers (CCBs) may have a positive influence on the long-term prognosis of Japanese patients with ischemic heart disease.

adalat 30mg tablets 2017-09-17

Little is known about the effect of nonsteroidal anti-inflammatory drugs (NSAIDs), thiazolidinediones (TZDs), nifedipine and nondihydropyridine calcium channel blockers (CCBs) usage on the risk of all-cause hospitalization among seniors with heart failure (HF). We assessed the risk of all-cause hospitalization associated with exposure to each of these drug classes, in a population of seniors with HF.Using the Quebec provincial databases, we conducted a nested case-control study in a population of individuals aged ≥65 with a first HF diagnosis between 2000 and 2009. Patients were considered users of a potentially inappropriate drug class if their date of hospital admission occurred in the interval between the date of the last drug claim and the end date of its days' supply. The risks of hospitalization were estimated using multivariate conditional logistic regression.Of the 128,853 individuals included in the study population, 101,273 (78 buy adalat .6%) were hospitalized. When compared to nonusers, users of NSAIDs (adjusted odds ratio: 1.16; 95% confidence interval: 1.13-1.20), TZD (1.09; 1.04-1.14), and CCBs (1.03; 1.01-1.05) had an increased risk of all-cause hospitalization, but not the users of nifedipine (1.00; 0.97-1.03).Seniors with HF exposed to a potentially inappropriate drug class are at increased risk of worse health outcomes. Treatment alternatives should be considered, as they are available.

adalat watch online 2017-01-24

To present the design of ACTION (A Coronary disease Trial Investigating Outcome with Nifedipine GITS), an ongoing multicentre clinical outcome trial with nifedipine GITS (Gastro-Intestinal Therapeutic System) in patients buy adalat with stable angina pectoris.

adalat r tablet 2015-07-25

While the intake of two oral contraceptives for 21 days did not influence the plasma concentration-time curve of unchanged nifedipine, mean AUC0-23.5 h and the mean Cmax values of dehydronifedipine were significantly lower in both groups tested/(24% in group A and 25% in group B). This observation may indicate a reduced formation rate of metabolites and reflects an inhibition of cytochrome P450 3A4 activity. The activation of the same or other metabolic degradation mechanism(s) could explain this buy adalat result.

tab adalat r 2015-02-24

A multinational, 70-centre, open-label study of N/C treatment for 28 or 52 weeks at a target dose of N60 mg/C32 mg. The primary assessment buy adalat included the incidence of treatment-emergent adverse events (TEAEs). Efficacy assessments included change from baseline in systolic and diastolic blood pressure (BP).

adalat medicine 2017-01-23

To evaluate the impact of extracellular and intracellular Ca2+ on contractions Celebrex Pain Medication induced by ethanol in smooth muscle.

adalat reviews 2015-09-17

We conclude, that the reduction in afterload did not Epivir Storage cause the typical changes in wave contour of the peripheral pulse curve which occur with organic nitrates. Most likely changes in the a/b ratio reflect changes in LV preload.

adalat 30 mg 2016-09-30

MCAs from DSS rats after stroke constricted in response to vasopressin but were unable to constrict in response to pressure or PDB in the presence of nifedipine, whereas those from DSS rats before stroke and from DSR rats constricted in response to all the stimuli. The PKC inhibitors, chelerythrine (12 micromol/l) and bisindolylmaleimide (5 micromol/l) inhibited constrictions in response to pressure and to Nexium Safe Dosage PDB in the presence of nifedipine.

adalat online 2015-11-04

Bone marrow-derived mesenchymal stem cells (BM- Esomeprazole Nexium Dose MSCs) can be induced to differentiate into myogenic cells. Despite their potential, previous studies have not been successful in producing a high percentage of cardiac-like cells with a muscle phenotype. We hypothesized that cardiac lineage development in BM-MSC is related to cell passage, culture milieu, and enrichment for specific cell subtypes before and during differentiation. Our study demonstrated that Lin(-) BM-MSC at an intermediate passage (IP; P8-P12) expressed cardiac troponin T (cTnT) after 21 days in culture. Cardiac TnT expression was similar whether IP cells were differentiated in media containing 5-azacytidine+2% FBS (AZA; 14%) or 2% FBS alone (LS; 12%) and both were significantly higher than AZA+5% FBS. This expression was potentiated by first enriching for CD117/Sca-1 cells followed by differentiation (AZA, 39% and LS, 28%). A second sequential enrichment for the dihydropyridine receptor subunit alpha2delta1 (DHPR-alpha2) resulted in cardiac TnT expressed in 54% of cultured cells compared to 28% of cells after CD117/Sca-1(+) enrichment. Cells enriched for CD117/Sca-1 and subjected to differentiation displayed spontaneous intracellular Ca(2+) transients with an increase in transient frequency and a 60% decrease in the transient duration amplitude between days 14 and 29. In conclusion, IP CD117/Sca-1(+) murine BM-MSCs display robust cardiac muscle lineage development that can be induced independent of AZA but is diminished under higher serum concentrations. Furthermore, temporal changes in calcium kinetics commensurate with increased cTnT expression suggest progressive maturation of a cardiac muscle lineage. Enrichment with CD117/Sca-1 to establish lineage commitment followed by DHPR-alpha2 in lineage developing cells may enhance the therapeutic potential of these cells for transplantation.

adalat cc medication 2017-11-18

NKA-mediated contraction of human colonic smooth muscle is Topamax Dosage dependent on an influx of extracellular Ca2+ through L-type voltage-operated Ca2+ channels. Intracellular Ca2+ release seems to have little role to play in NKA-mediated contractions.

adalat pills 2016-05-01

The human hypothalamic hamartoma (HH) is a rare, intrinsically epileptogenic lesion associated with gelastic seizures, but the underlying mechanisms Cialis Online remain unclear. Here, we examined the role of GABAA receptors in surgically resected HH tissue.

adalat 60 mg 2017-07-24

Ca(2+)/calmodulin-dependent protein kinase IV (CaM kinase IV) is a multifunctional enzyme that is abundantly present in the nuclei of neurons. We report the properties of phosphorylation and activation of CaM kinase IV in comparison to CaM kinase II in cultured rat hippocampal neurons. Phosphorylation and activity of CaM kinase IV as well Lipitor Reviews Webmd as CaM kinase II were increased by treatment of neurons either with glutamate or high K(+). Glutamate-induced phosphorylation and activity of CaM kinase IV were blocked by N-methyl-D-asparate (NMDA) antagonists, and NMDA application instead of glutamate did increase CaM kinase IV phosphorylation. CaM kinase IV phosphorylation was also increased by alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA), and was blocked by an inhibitor of NMDA receptor. The AMPA-induced phosphorylation was blocked by tetrodotoxin, a Na(+) channel blocker, that was expected to block endogenous glutamate transmission indirectly. On the other hand, high K(+)-induced phosphorylation and activation were not blocked by inhibitors of glutamate receptors, and effectively blocked by nifedipine, an L-type Ca(2+) channel blocker. These properties were similar between CaM kinase IV and CaM kinase II.

adalat storage 2016-11-07

We performed a randomized, double-blind multi-centre study, to compare the safety, efficacy and tolerability of an intravenous (i.v.) infusion of two dihydropyridine calcium Online Order Viagra channel blockers (either nifedipine or felodipine) in 122 patients, of whom 63 were diagnosed as hypertensive emergencies and 59 as hypertensive crisis, who had not reacted adequately (diastolic blood pressure <115 mmHg) to 5 mg of nifedipine PO.

adalat drug 2017-10-08

Secretion of LH from gonadotropes is initiated by a GnRH-induced increase in intracellular Ca(2+) concentration ([Ca(2+)](i)). This increase in [Ca(2+)](i) is the result of Ca(2+) release from intracellular stores and Ca(2+) influx through voltage-dependent Ca(2+) channels. Here we describe an ether-à-go-go-related gene (erg) K(+) current in primary mouse gonadotropes and its possible function in the control of Ca(2+) influx. To detect gonadotropes, we used a knock-in mouse strain, in which GnRH receptor-expressing cells are fluorescently labeled. Erg K(+) currents were recorded in 80-90% of gonadotropes. Blockage of erg currents by E-4031 depolarized the resting potential by 5-8 mV and led to an increase in [Ca(2+)](i), which was abolished by nifedipine. GnRH inhibited erg currents by a reduction of the maximal erg current and in some cells additionally by a shift of the activation curve to more positive potentials. In conclusion, the erg current contributes to the maintenance of the resting potential in gonadotropes, thereby securing a low [Ca(2+)](i) by restricting Ca(2+) influx. Artane Medication Uses In addition, the erg channels are modulated by GnRH by an as-yet unknown signal cascade.