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A 71-year-old woman experienced an acute onset of angioedema and a photosensitive pruritic rash after 3 months of therapy with valsartan, an angiotensin II receptor antagonist. After discontinuing valsartan and treatment with subcutaneous epinephrine, intravenous methylprednisolone, diphenhydramine, and Eucerin cream, her symptoms dissipated and the rash resolved. Rash and angioedema have been reported with angiotensin-converting enzyme inhibitors and, very rarely, with losartan, the other currently marketed angiotensin II receptor antagonist. To our knowledge, this is the first report of such a reaction with valsartan.
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Blacks appear to have a more modest blood pressure (BP) response to angiotensin receptor blocker (ARB) monotherapy than non-Blacks. This post-hoc analysis compared the BP-lowering efficacy of olmesartan medoxomil (OM), losartan potassium (LOS), and valsartan (VAL) in Black versus non-Black participants in a randomized, forced-titration study. Patients were randomized to OM 20, LOS 50, and VAL 80mg/day or placebo for 4 weeks and uptitrated to 40, 100, and 320mg/day doses, respectively, by study end. The primary end point was the mean change from baseline in diastolic BP (DBP) at week 8. All treatments produced significant reductions in mean DBP and systolic BP (SBP) in Blacks (n=150; P < .001). BP <140/90mm Hg was achieved in 35.0%, 15.6%, 29.7%, and 5.0% of Blacks receiving OM, LOS, VAL, and placebo, respectively, and in 41.0%, 21.1%, 28.8%, and 14.5% of non-Blacks receiving OM, LOS, VAL, and placebo, respectively, after 8 weeks. BP-lowering efficacy of the three agents was similar at 3 months. OM had the greatest early efficacy, with numerically greater mean reductions in DBP and SBP, and a higher proportion of Black and non-Black patients achieving goal BP of 140/90mm Hg at week 8.
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Despite significant therapeutic advances, patients with chronic heart failure (HF) remain at high risk of morbidity and mortality. Sacubitril valsartan (previously known as LCZ696) is a new oral agent approved for the treatment of symptomatic chronic heart failure in adults with reduced ejection fraction. It is described as the first in class angiotensin receptor neprilysin inhibitor (ARNI) since it incorporates the neprilysin inhibitor, sacubitril and the angiotensin II receptor antagonist, valsartan. Neprilysin is an endopeptidase that breaks down several vasoactive peptides including natriuretic peptides (NPs), bradykinin, endothelin and angiotensin II (Ang-II). Therefore, a natural consequence of its inhibition is an increase of plasmatic levels of both, NPs and Ang-II (with opposite biological actions). So, a combined inhibition of these both systems (Sacubitril / valsartan) may enhance the benefits of NPs effects in HF (natriuresis, diuresis, etc) while Ang-II receptor is inhibited (reducing vasoconstriction and aldosterone release). In a large clinical trial (PARADIGM-HF with 8442 patients), this new agent was found to significantly reduce cardiovascular and all cause mortality as well as hospitalizations due to HF (compared to enalapril). This manuscript reviews clinical evidence for sacubitril valsartan, dosing and cautions, future directions and its considered place in the therapy of HF with reduced ejection fraction.
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Angiotensin II can induce cardiac fibrosis, stimulate cardiac fibroblast proliferation and extracellular matrix synthesis, while Xuefu Zhuyu Decoction can prevent cardiac fibrosis, the mechanism of which may be related to inhibiting CF proliferation and extracellular matrix synthesis.
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To observe the effects of angiotensin converting enzyme inhibitors (ACEI) and angiotensin II receptor blocker (ARB) on tumor growth and angiogenesis in implanted gastric cancer mouse model, and to explore the probable mechanism of ACEI and ARB anticancer effect.
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We conducted an open-label, randomized trial to compare the effects of aliskiren with those of valsartan. Patients with BP <150/90 mmHg, an estimated glomerular filtration rate of 90-30 mL/min/1.73 m(2), and albuminuria >30 mg/g, despite treatment with a 160 mg daily dose of valsartan, were randomly assigned to the following two groups: the aliskiren group, who switched from 160 mg/day valsartan to 150 mg/day aliskiren, which was later increased to 300 mg/day (n = 20); and the valsartan group, who continued with 160 mg/day valsartan (n = 20).
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Compared with control group, rabbits treated with L-Thy only were found to have remarkable myocardial hypertrophy and extracellular matrix fibrosis. Increased plasma and tissue AngII were detected in L-Thy group. RT-PCR and Western blotting analysis revealed enhanced mRNA and protein expression of ACE, AT1R and AT2R. It was also demonstrated that both imidapril and valsartan alleviated cardiac hypertrophy and extracellular matrix fibrosis induced by L-Thy. Compared with L-Thy and valsartan group, imidapril group showed significantly lower plasma /tissue AngII concentration and more effective inhibition of extracellular matrix fibrosis. Imidapril did not alter the expression of ACE, AT1R or AT2R. Plasma concentration of AngII was markedly higher in valsartan group compared with L-Thy group, whereas tissue AngII concentration showed no significant difference between two groups. In valsartan group, AT1R and AT2R mRNA expressions were significantly upregulated, whereas valsartan did not change mRNA and protein expression of ACE.
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Both aging and hypertension could result in excessive proliferation of rat aortic VSMCs and the expression changes of correlated cytoactive factors. The extracts from Panax ginseng, Panax notoginseng (Burk.) and Ligusticum chuanxiong can lower their proliferation levels and reduce the expressions of negative cytokines, thus reducing aging and hypertension induced injury of VSMCs and delaying angiocellular aging.
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LCZ696 is superior to valsartan alone in reducing blood pressure. Preliminary results from a Phase II trial showed that LCZ696 reduced NT-proBNP to a greater extent than valsartan alone, and in addition LCZ696 had beneficial effects on symptoms. With these promising first results, the results of ongoing further studies in heart failure are eagerly awaited.
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The combination of amlodipine/valsartan in this 8-week double-blind study provided additional BP control and was well tolerated in patients inadequately controlled with amlodipine monotherapy. Results should be interpreted with the knowledge that study entry criteria may limit application to a wider population.
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Angiotensin II receptor blockers (ARBs) are widely used as hypertensive therapeutic agents. However, it has been reported that Telmisartan (a type of ARB) additionally activates peroxisome proliferator-activated receptor (PPAR)-γ. We previously reported that PPAR-γ ligand induced the growth arrest of renal cell carcinoma (RCC) cells through apoptosis, and that Telmisartan had the potential to inhibit prostate cancer cell growth through apoptosis. In this study, we evaluated the effects of Telmisartan and other ARBs on cell proliferation in an RCC cell line using normal proximal tubular endothelial cells (PRTECs) and the human RCC (Caki-1) cell line. The effects of Telmisartan as well as of other ARBs (Candesartan, Valsartan, Irbesartan and Losartan) on RCC cell growth were examined by MTT assay. Flow cytometry and Hoechst staining were used to determine whether or not the ARBs induced apoptosis. Telmisartan caused marked inhibition in RCC cells in a concentration- and time-dependent manner. Treatment with 100 µM of Telmisartan induced early apoptosis and DNA fragmentation in the RCC cells, but not in the PRTECs. None of the other ARBs had an effect on cell proliferation in the RCC cells or the PRTECs. Telmisartan may mediate potent antiproliferative effects against RCC cells through PPAR-γ. Thus, Telmisartan is a potential target for prevention and treatment in RCC.
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To observe the effect of valsartan on brian ultrastructure, Klotho gene and micro-inflammatory factor [intercellular adhesion molecule-1(ICAM-1) and vascular cell adhesion molecule-l(VCAM-1)] expression in spontaneously hypertensive rat models.
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Sustained ventricular arrhythmias and heart failure are well-recognized complications after acute myocardial infarction (AMI) and have been associated with worse outcomes and increased mortality. The use of and outcomes associated with acute beta-blocker therapy in patients with AMI complicated by sustained ventricular tachycardia (VT) or ventricular fibrillation (VF) and heart failure were investigated. Of 5,391 patients in the VALIANT Registry, sustained VT/VF occurred in 306 (5.7%), with an in-hospital mortality rate of 20.3%. Multivariable logistic regression identified sustained VT/VF as a major predictor of in-hospital death (relative risk 4.18, 95% confidence interval 2.91 to 5.93). Of those with sustained VT/VF, 55.2% were treated with intravenous or oral beta blockade in the first 24 hours. After adjusting for baseline characteristics, propensity for acute beta-blocker use, and the interaction between Killip classification and beta-blocker therapy, beta-blocker therapy within 24 hours was associated with decreased in-hospital mortality in patients with sustained VT/VF (relative risk 0.28, 95% confidence interval 0.10 to 0.75, p = 0.013) without evidence of worsening heart failure. Patients with sustained VT/VF were less likely to receive beta blockers within 24 hours (p = 0.001). In conclusion, sustained VT/VF was common after AMI. In patients with sustained VT/VF, beta-blocker therapy in the first 24 hours after AMI was associated with decreased early mortality without worsening heart failure. Unfortunately, beta blockers were underused acutely in patients with sustained VT/VF.
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Inhibition of the renin-angiotensin-aldosterone system plays a pivotal role in the prevention and treatment of diabetic nephropathy. Angiotensin II receptor blockers (ARB) exert a renoprotective effect and attenuate the progression of diabetic nephropathy. However, the underlying cellular and molecular mechanisms in the kidney remain to be elucidated. The present study was undertaken to focus on the effect of local angiotensin II type 1 receptor blockade on the inflammatory reaction during the early stages of diabetic nephropathy.
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To observe the accumulation of dendritic cells (DCs) in rat remnant kidney and its contribution to tubulointerstitial fibrosis, under influence of valsartan on DCs, a rat remnant kidney model was established by subtotal nephrectomy. Four experimental groups were included: normal, sham, model (SNx) and the group treated with Valsartan (SNxV). Rats were killed at week 1, 4 and 12, respectively. CD1a+CD80+ DCs were assayed by double immunostaining method and the images were analyzed with Axioplan 2 microscopy. The expressions of P-selectin, TGF-beta1, alpha-SMA, collagen III and fibronectin was analyzed by immunohistochemistry or semi-quantitative RT-PCR, and the level of tubulointerstitial firosis (TIF) was scored. CD1a+CD80+ DCs were gradually increased among renal tubules, interstitium and vessels, especially in interstitium, and the number of DCs in model group at week 12 was much more than that in model groups at week 1 or 4. The expressions of P-selectin, TGF-beta1, alpha-SMA, collagen III and fibronectin in tubulointerstitial areas and the degree of TIF was increased substantially in model group at week 12. The accumulation of DCs in interstitium was well associated with the loss of renal function and the progression of tubulointerstitial fibrosis. Valsartan treatment inhibited the local accumulation of DCs and attenuated renal tubulointerstitial damage. The local DCs accumulation was related to tubulointerstitial fibrosis and renal dysfunction following renal ablation. Blockade to angiotensin II might be a potent way to attenuate renal immuno-inflammatory injury.
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The frequencies of the genotypes DD and ID were higher in the DKD+ than in the DKD- group. The frequency of allele D was higher, and of allele I was lower, in the DKD+ than in DKD- group (p < 0.05). Following valsartan treatment, albuminuria was significantly decreased in subgroups DD and ID (p < 0.05).
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To develop an easy assay for the quantitation of the angiotensin II receptor antagonist valsartan in human plasma using a liquid extraction procedure.
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Val-HeFT was a randomized, double-blind parallel-arm study in which HF patients (New York Heart Association class II-IV) received either valsartan (n = 2511, force-titrated to 160 mg twice daily) or placebo (n = 2499) in addition to prescribed HF therapy. Total and per patient-year investigator-assessed hospitalizations (all-cause or HF) were analyzed according to prescribed therapy at baseline (angiotensin-converting enzyme inhibitors [ACEI] and beta-blockers [BB]).
Angiotensin II receptor blockers (ARBs) vary in their binding affinities to angiotensin II type 1 (AT(1)) receptors in in vitro experiments. We compared a high-affinity ARB, olmesartan, and a low-affinity ARB, valsartan, in terms of their vascular protective effects in stroke-prone spontaneously hypertensive rats (SHR-SP). Blood pressure was equally reduced by placebo, olmesartan (1 mg kg(-1)) and valsartan (3 mg kg(-1)) daily for 2 weeks. In another experiment, 12-week-old SHR-SP were fed 8% salt, and olmesartan (1 mg kg(-1)), valsartan (3 mg kg(-1)) or placebo were administered daily until a survival rate of 60% was reached. In the experiment using SHR-SP, the reduction of acetylcholine-induced vascular relaxation and the increase of p22(phox) expression in the placebo-treated group were significantly attenuated by olmesartan and valsartan, but this attenuation was significantly greater for olmesartan. In immunohistological analysis, all areas positive for angiotensin II, p22(phox) and 4-hydroxy-2-nonenal were significantly reduced by olmesartan and valsartan, but again this reduction was significantly greater for olmesartan. In salt-loaded SHR-SP, the number of days to reach a 60% survival rate was 25 and 42 in placebo and valsartan-treated rats, respectively, and this represented a significant difference. The survival rate in olmesartan-treated rats was 95% at day 42, when valsartan-treated rats reached 60% survival, and this difference was also significant. In the surviving rats, olmesartan, but not valsartan, augmented acetylcholine-induced vascular relaxation and attenuated vascular p22(phox) expression. Thus, heterogeneity in binding affinity to AT(1) receptors among ARBs may result in different degrees of vascular protection and lifespan extension.
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In Sprague-Dawley rats, we used a closed cranial window preparation to measure changes in pial vessel diameters following topical acetylcholine (ACh) before smoking. After one-minute smoking, we again examined the arteriolar responses to ACh. Finally, after intravenous fasudil or apocynin pre-treatment we re-examined the vasodilator responses to topical ACh (before and after cigarette smoking).