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Valsartan, a selective angiotensin II type 1 receptor (AT1R) blocker, has beneficial effects in the cardiovascular system in part by its increase of nitric oxide (NO) bioavailability, yet the mechanisms are unclear. We investigated the molecular mechanisms underlying this effect in endothelial cells (ECs).
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To compare the inhibitory potency of candesartan, valsartan, eprosartan and embusartan in blocking presynaptically and postsynaptically located AT1 receptors.
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To evaluate the long-term tolerability and efficacy of the amlodipine/valsartan 5/320 mg once daily (o.d.) combination in hypertensive patients.
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We investigated pleiotropic features of azilsartan in cell-based assay systems independent of its effects on blood pressure. In cultured 3T3-L1 preadipocytes, azilsartan enhanced adipogenesis and exerted greater effects than valsartan on expression of genes encoding peroxisome proliferator-activated receptor-α (PPARα), PPARδ, leptin, adipsin, and adiponectin. The effects of azilsartan on adipocyte differentiation and gene expression were observed at concentrations of azilsartan that did not classically stimulate PPAR activity in cell-based transactivation assays. Azilsartan also potently inhibited vascular cell proliferation in the absence of exogenously supplemented angiotensin II. In aortic endothelial cells, azilsartan inhibited cell proliferation at concentrations as low as 1 μmol/l, whereas valsartan showed little or no antiproliferative effects at concentrations below 10 μmol/l. Antiproliferative effects of azilsartan were also observed in cells lacking AT1 receptors. In addition, azilsartan, but not valsartan, blocked angiotensin II-induced activation of mitogen-activated protein kinase in vascular smooth muscle cells 4-8 h after washout of drug from the incubation media.
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New diabetes was reported in 580 (11.5%) patients on valsartan and in 718 (14.5%) patients on amlodipine (OR 0.77, 95% CI 0.69-0.87, P < 0.0001). Using stricter criteria (without adverse event reports) new diabetes was detected in 495 (9.8%) patients on valsartan and in 586 (11.8%) on amlodipine (OR 0.82, 95% CI 0.72-0.93, P = 0.0015).
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Based on the literatures published, it has been demonstrated that pharmacokinetic interactions of losartan with other agents are mainly via CYP2C9- and CYP3A4-mediated, the role played by CYP enzyme system in the metabolism of valsartan, candesartan, irbesartan, and azilsartan appears modest, and cytochrome P450 system has no influence on the metabolism of telmisartan, eprosartan, olmesartan. Therefore, according to these pharmacokinetic findings, no dosage adjustment is recommended when eprosartan, telmisartan and olmesartan are combined with other pharmacological agents in patients with hypertension.
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The binding characteristics of the angiotensin AT1 receptor antagonist valsartan were investigated in different animal species and tissues. Using [125I](Sar1,Ile8) angiotensin II as radioligand, affinity constants were determined in liver and adrenal rat and marmoset, human adrenal and in rat aortic smooth muscle cells. In all tissues tested, valsartan had a greater affinity for the AT1 receptor than losartan (on average 5-fold). The affinities of both antagonists were up to 30 times weaker in the dog tissues [3H]Valsartan bound with high affinity (Kd 1.44 nmol/l) to the rat aortic smooth muscle cell AT1 receptor. Binding was saturable and reversible. Non-specific binding was low (10%). Reports that [3H]losartan binds to a non-angiotensin II binding site in rat liver and in other tissues could be confirmed. [3H]Valsartan on the other hand bound only to the AT1 receptor. Using a competition binding assay with [3H]losartan on rat liver membranes it could be shown that valsartan can bind to the 'losartan binding site', but at a 10,000-fold less affinity than for the AT1 receptor. Valsartan is therefore a highly specific and selective antagonist of the AT1 receptor. Due to its high affinity and low non-specific binding it is a suitable radioactive antagonist for the study of the distribution and function of the angiotensin AT1 receptor.
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This retrospective, propensity score-matched study evaluated patients switching to a single-pill combination of valsartan-hydrochlorothiazide in RP compared with patients remaining on the combination without reminder packaging (non-RP). Patients receiving combination therapy between April 1, 2009 and July 31, 2010 were eligible for inclusion. Patients were propensity score-matched on baseline adherence and background demographic variables, including comorbidities. Medication possession ratio, proportion of days covered, time to refill, and time to discontinuation were evaluated as primary measures of subsequent adherence and persistence.
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We previously reported that acute cigarette smoking can cause a dysfunction of endothelium-dependent vasodilation in cerebral vessels, and that a reduction of oxidative stress by agents such as valsartan, fasudil, or apocynin prevented this impairment. Here, our aim was to investigate the comparative effects of two antiplatelet drugs used for stroke-prevention [a phosphodiesterase-3 inhibitor (cilostazol) and a cyclooxygenase inhibitor (aspirin)] on smoking-induced endothelial dysfunction in cerebral arterioles. In Sprague-Dawley rats, we used a closed cranial window preparation to measure the changes in pial vessel diameters induced by topical application of acetylcholine (ACh) following intraperitoneal injection of 0.5% carboxymethyl cellulose sodium salt (CMC; vehicle control for the antiplatelet drugs). After 1-min smoking (1 mg-nicotine cigarette), the arteriolar responses to ACh were reexamined. Finally, after intraperitoneal cilostazol or aspirin (each in 0.5% CMC) pretreatment, we reexamined the vasodilator responses to topical ACh (before and after cigarette smoking). Under control conditions, cerebral arterioles were dose-relatedly dilated by topical ACh (10(-6) and 10(-5 )M). One hour after 1-min smoking, 10(-5 )M ACh (a) constricted cerebral pial arterioles in the control group and in the aspirin-pretreatment group (responses not significantly different from each other), but (b) dilated cerebral pial arteries in the cilostazol pretreatment groups (responses significantly different from those obtained without cilostazol pretreatment). Thus, cilostazol (but not aspirin) may prevent the smoking-induced impairment of endothelium-dependent vasodilation in cerebral pial arterioles.
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The aim of this study was to compare the cost-utility of the first available single-pill triple combination antihypertensive therapy containing valsartan (V), amlodipine (A) and hydrochlorothiazide (H), with each of the same components dual combinations in patients with moderate to severe hypertension. A Markov model with eight health states was constructed. The short-term effect of antihypertensive treatment on blood pressure was extrapolated through the Hellenic SCORE and Framingham risk equations, estimating the long-term survival and quality-adjusted life-years (QALYs) saved. Costs and outcomes were evaluated over lifetime, divided into annual cycles and discounted at 3.0 % with 2013 as reference year. The analysis was conducted by the Greek third-party-payer perspective. The triple combination treatment cost was estimated at €16,525 compared to €15,480 for V/A, €14,125 for V/H and €11,690 for A/H. The QALYs saved with the triple combination were 12.76 vs. 12.64, 12.61 and 12.38 for double combinations respectively. The incremental cost-effectiveness ratio of the triple combination versus V/A and A/H was far lower than the Greek GDP per capita (€8,690/QALY and €12,695/QALY, respectively) and really close for V/H (€16,192/QALY), suggesting V/A/H combination to be cost-effective. Extensive sensitivity analyses confirmed the robustness of the results. The probability that the triple combination is cost effective was more than 90 % at a willingness-to-pay threshold of €18,000/QALY. This is the first study to evaluate the cost-utility of a single-pill triple combination. The single-pill V/A/H therapy is a cost-effective antihypertensive choice for the treatment of moderate to severe hypertension, compared to its dual components.