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Alcohol promotes the myocardial oxidative stress and fibrosis through an elevated expression of PYK2 and a lowered expression of caveolin-1. Then a deterioration of cardiac structures and functions occur.
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The objectives of this trial are to observe BP reduction, compliance and regimen changes 3 months after initiation of valsartan alone or with hydrochlorothiazide and optimized patient support.
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Angiotensin II (AT II) is a final product of the renin-anglotensin-aldosterone system (RAS) and presents one of the most influential factors in the pathogenesis of atherosclerosis, acute coronary syndrome, myocardial dysfunction and heart failure. ACE-inhibitors (ACEI), beside beta adrenergic blockers, are a cornerstone of the current chronic heart failure (CHF) treatment. Evidence based medicine has not yet proved any significant beneficial effects of ACEI in patients with unstable angina pectoris (UAP), although according to the SoLVD study testing the possible effects of ACEI in patients with significant left ventricular dysfunction and/or CHF, there was a significant hospitalization rate reduction as well as less transformation of UAP to myocardial infarction in patients treated with ACEI. In the GISSI 3, ISIS 4 and CCS studies, ACEI was given within the first 24 hours and continued for 4-6 weeks. According to pooled results, ACE inhibitor could save 11/1000 patients with ST-elevation myocardial infarction (STEMI) and only 1/1000 patients with non ST-elevation myocardial infarction (NSTEMI). In the SAVE, AIRE and TRACE studies, ACEI was started later, i.e. 3-16 days after acute myocardial infarction and continued for several years. ACEI therapy resulted in a significantly lower mortality during the first year, and an even 20% relative reduction in the total mortality during the 4-year follow up. The effects of ACEI were even more prominent in more severe myocardial dysfunction, as it was well known that they could slow or stop unfavorable myocardial remodeling. Conclusively, ACEI should be given as early as possible to all patients with acute myocardial infarction, if no contraindications. The HOPE study showed efficacy of ACEI in the primary prevention of ischemic heart disease in high risk individuals, and the EUROPA study showed a favorable effect of ACEI in the secondary prevention of ischemic heart disease in low risk patients. According to these findings, ACEI should be given permenantly following myocardial infarction. These findings suggest the need of a permanent treatment with ACEI in patients having sustaned myocardial infarction. Angiotensin-1 receptor antagonists (AT-1 antagonists) are a newer generation of neurohormonal antagonists, which block the effects of AT II produced not only through a classic, ACE-dependent pathway but also via alternative pathways (non ACE-dependent) and selectively bind to AT-1 receptors for AT II. Therefore, they have some theoretical advances in comparison with ACEI. There are 2 relevant studies elucidating their possible role in treating patients with or post-myocardial infarction. The OPTIMAAL study did not prove losartan to be better than an ACEI (captopril), while the VALIANT study showed that the effects of valsartan vs. captopril were statistically nonsignificantly different. Furthermore, there is no sense to combine AT-1 antagonist and ACEI, while a combination of AT-1 antagonist and a beta blocker is justified. In other words, AT-1 antagonist (the class effect is disputable) should be given to patients with acute myocardial infarction or to post-myocardial infarction patients who cannot take ACEI.
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A clinical trial showed comparable blood pressure (BP) lowering by valsartan/hydrochlorothiazide and amlodipine/hydrochlorothiazide in obese hypertensive patients. Relative to amlodipine/hydrochlorothiazide, valsartan/hydrochlorothiazide reduced the hyperglycemic response to glucose challenge. An objective of this post hoc analysis was to determine whether this benefit extended to African Americans and whites. Treatments (160/12.5 mg of valsartan/hydrochlorothiazide force titrated to 320/25 mg of valsartan/hydrochlorothiazide at week 4 or 12.5 mg of hydrochlorothiazide force titrated to 25 mg of hydrochlorothiazide at week 4 with 5 and 10 mg of amlodipine added at weeks 8 and 12, respectively) were administered once daily. Both treatments reduced clinic BP from baseline to all visits (P < 0.0001), regardless of race/ethnicity (126 African Americans, 212 whites). In African Americans, there were no significant between-treatment differences in clinic or ambulatory BP lowering at weeks 8 or 16. Whites responded better to valsartan/hydrochlorothiazide. In both racial/ethnic subgroups, the addition of valsartan but not amlodipine mitigated the hyperglycemic response to hydrochlorothiazide through enhanced insulin secretion. Valsartan/hydrochlorothiazide was as effective as amlodipine/hydrochlorothiazide was in reducing BP in obese, hypertensive African Americans and better than amlodipine/hydrochlorothiazide in whites. In both racial/ethnic subgroups, the addition of valsartan to hydrochlorothiazide reduced the negative metabolic effects associated with thiazide therapy.
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Approximately 3 days a month, some 15% to 20% of patients with hypertension do not recall having taken their antihypertensive medication. Individuals with this frequency of missed doses may be at increased risk for a cardiovascular event and may have a poorer long-term prognosis.
Heart failure (HF) impacts an estimated 5.7 million Americans, and its prevalence is projected to increase to more than 8 million Americans in the next 15 years. Key clinical trials have established an evidence-based foundation for treatment of heart failure with reduced ejection fraction (HFrEF). Ivabradine and sacubitril/valsartan, which inhibit the f-channel and the angiotensin receptor and neprilysin, respectively, were recently approved by the Food and Drug Administration for HFrEF. In systolic heart failure, treatment with the If inhibitor ivabradine significantly reduced the combined endpoint of cardiovascular mortality or heart failure hospital admission vs placebo (P < .05). In the Prospective Comparison of angiotensin receptor-neprilysin inhibitor (ARNI) with angiotensin-converting enzyme inhibitor (ACEI) to Determine Impact on Global Mortality and Morbidity in Heart Failure trial, sacubitril/valsartan significantly reduced the combined endpoint of cardiovascular death or heart failure hospitalization vs enalapril (P < .001). The place of therapy with ivabradine and sacubitril/valsartan is defined by these trials and their interplay with guideline-directed medical therapy. Ivabradine and sacubitril/valsartan increase pharmacotherapy options for the treatment of HFrEF but are not yet first-line agents. Clinical application will be better defined in the coming years as practitioners increase their familiarity with ivabradine and sacubitril/valsartan.
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Angiotensin II receptor blockers (ARBs) are widely used in the treatment of patients with hypertension, heart failure, diabetic nephropathy and other clinical conditions. Several intervention trials and systematic overviews showed that both angiotensin-converting enzyme inhibitors and ARBs effectively reduce the risk of stroke, myocardial infarction and congestive heart failure in hypertensive patients. Two recent intervention trials conducted in Japan (JIKEI and Kyoto studies) suggested that the protective effect of ARBs on major cardiovascular events might be partly independent from the degree of blood pressure (BP) reduction. Both studies used a prospective randomized open blinded end point (PROBE) design. No significant differences emerged in both studies between the ARB group (valsartan) and the control group in the achieved BP. We made a pooled analysis of the JIKEI and Kyoto studies. Overall, valsartan significantly reduced the risk of the primary composite outcome (by 42%; P<0.0001), angina pectoris (by 38%; P<0.0001), heart failure requiring hospitalization (by 43%; P=0.013) and cerebrovascular events (by 42%; P=0.002). The protective effect on the dissecting aneurysm of aorta bordered statistical significance. These data reinforce the notion that the protective effect of angiotensin II inhibition is partly independent of BP reduction.
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The blood pressure level of patients with TGF-beta 1 gene +869 CC genotype, TT genotype, TC genotype showed no significant difference (P> 0.05) before treatment. The urinary MA level of the three genotypes was CC genotype's > TC genetype's > TT genotype's in sequence, and the urinary MA level of CC genotype was significantly higher than that of TC genotype and of TT genotype (P< 0.01). The serum levels of TGF-beta1 in the three genotypes was CC genotype's > TC genotype's > TT genotype's in sequence (P< 0.01). There was statistically significant positive correlation between the urinary MA level and the serum level of TGF-beta1(P< 0.05). After 8 weeks treatment with valsartan, there was significant decrease of the blood pressure, the urinary MA level, and the serum level of TGF-beta1. However, the blood pressure reduction of the three types had no statistical significant difference in sequence. The absolute value of urinary MA reduction was CC genotype's > TC genotype's > TT genotype's in sequence, the reduction absolute value of urinary MA in CC genotype was higher than that of TC genotype and of TT genotype (P< 0.05), but the reduction percentage of the urinary MA in the three genotypes showed no statistically significant difference (P> 0.05). The reduction of serum levels of TGF-beta1 was CC genotype's > TC genotype's > TT genotype's in sequence, there was significant difference between each other (P< 0.01). However, the reduction percentage of the serum level of TGF-beta 1 in the three types showed no statistically significant difference (P> 0.05).
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Thirty-six male Wistar rats were randomly divided into the following three groups with twelve rats in each group: control group, surgery (model) group, and valsartan group. Aortic balloon injury was performed to elicit endothelial denudation with a 2F balloon catheter. On days 14 and 28 after injury, blood was harvested to measure bilirubin levels. Aortic arteries were harvested for morphometry analysis, to determine angiotensin II (Ang II) level, and to analyze mRNA or protein expression.
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ARBs are an important therapy for hypertensive type 2 diabetic patients and can benefit normotensive diabetic patients as well. ARB dosage optimization or the addition of a second renoprotective agent (ACE inhibitor or non-dihydropyridine calcium-channel blocker) may be important for optimal renoprotection, although further research is clearly needed in this area.
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Little is known about the effects of the pro-inflammatory hormone Angiotensin II (Ang II) in inflammatory bowel disease. The aim of this study was to evaluate the effect of valsartan (Diovan), an Ang II receptor antagonist, in two models of colitis.
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This was a randomised, open, three-way crossover study in 12 healthy male volunteers to determine the effect of a single oral dose of cimetidine on the pharmacokinetics of a single oral dose of the angiotensin II receptor antagonist valsartan and vice versa. The volunteers received either valsartan alone (160 mg), or cimetidine alone (800 mg), or valsartan 1 h after cimetidine. The study was designed primarily to detect a possible influence of cimetidine on the rate and extent of absorption of valsartan.
To compare the level of expression of the renin-angiotensin-aldosterone system (RAAS) in mice with or without the endothelin-1 receptor antagonist bosentan and to examine the potential value in blood pressure regulation.
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The plasma glucose concentration was assessed by the glucose oxidase method. The concentration of beta-endorphin in plasma or medium incubating adrenal medulla was measured using an enzyme-linked immunosorbent assay. The mRNA levels of the subtype 4 form of glucose transporter (GLUT4) in soleus muscle and phosphoenolpyruvate carboxykinase (PEPCK) in the liver were detected by Northern blotting analysis, while the protein levels of GLUT4 in isolated soleus muscle and hepatic PEPCK were investigated using Western blotting analysis.
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Primary myocardial cells were seperated and cultured together with angiotensin II (Ang II) for 72 or 96 hours. The total protein content with the BCA method and the photography and measurement of cell diameter with inverted microscope reflected myocardial cell proliferation. The mitochondrial membrane potential (Delta Psi m) with fluorescence microscope, the mitochondrial single amine oxidase (MAO) activity with spectrophotometer, the mitochondrial cytochrome oxidase (COX) activity and the injury percentage of mitochondrial outer membrane with microplate reader and the contents of ATP, ADP, AMP with high performance liquid chromatography reflected the injury and energy metabolism of myocardial cell mitochondrial structure and function when being cultured together with Ang II. On that basis, cells were treated with Astragali Radix injection and valsartan for observing pharmacological effects on mitochondrial structure and function in restructured myocardial cells.
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Sudden death (SD) is a frequent catastrophic complication in patients after myocardial infarction. Circumstances of SD may affect strategies for prevention.
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The objective of this work was to develop a population pharmacokinetic model to assess the influence of subject covariates on the pharmacokinetics of valsartan in children. Data were collected from a single dose study in 26 hypertensive children ages 1 to 16 years. Subjects received 2 mg/kg valsartan suspension up to a maximum dose of 80 mg. Plasma samples were collected and analyzed using LC/MS/MS. Several structural pharmacokinetic models were evaluated for appropriateness. Allometric scaling and standard covariate analyses were performed to explain interindividual variabilities. Objective function values and goodness of fit plots were used for model selection. A posterior predictive check was used for model evaluation. A linear 2-compartment first-order elimination model with zero-order absorption and lag-time best described the disposition of valsartan. Allometric scaling and standard covariate analysis revealed that age and body size have similar influence; however, after adjustment for body size using fat free mass (FFM), the effect of increasing age was no longer significant on valsartan clearance (2% per year relative to a typical 8 year old with FFM of 30 kg). The population pharmacokinetic model reveals that increase in age has minimal influence on body size dependent clearance of valsartan in children.
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The relative efficacy of antihypertensive drugs/combinations is not well known. Identifying the most effective ones and the patients' characteristics associated with best performance of the drugs will improve management of hypertensive patients.
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These results suggested that the inhibiting effect of RGS2 on VSMC proliferation is downregulated in vascular remodeling of injured rat aorta, and this effect is likely to be mediated by angiotensin II signaling.
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This study investigated the process of nitric oxide (NO) release from platelets after stimulation with different angiotensin II type 1 (AT1)-receptor antagonists and its effect on platelet adhesion and aggregation. Angiotensin II AT1-receptor antagonist-stimulated NO release in platelets was compared with that in human umbilical vein endothelial cells by using a highly sensitive porphyrinic microsensor. In vitro and ex vivo effects of angiotensin II AT1-receptor antagonists on platelet adhesion to collagen and thromboxane A2 analog U46619-induced aggregation were evaluated. Losartan, EXP3174, and valsartan alone caused NO release from platelets and endothelial cells in a dose-dependent manner in the range of 0.01 to 100 micro mol/L, which was attenuated by NO synthase inhibitor N(G)-nitro-L-arginine methyl ester. The angiotensin II AT1-receptor antagonists had more than 70% greater potency in NO release in platelets than in endothelial cells. The degree of inhibition of platelet adhesion (collagen-stimulated) and aggregation (U46619-stimulated) elicited by losartan, EXP3174, and valsartan, either in vitro or ex vivo, closely correlated with the NO levels produced by each of these drugs alone. The inhibiting effects of angiotensin II AT1-receptor antagonists on collagen-stimulated adhesion and U46619-stimulated aggregation of platelets were significantly reduced by pretreatment with N(G)-nitro-L-arginine methyl ester. Neither the AT2 receptor antagonist PD123319, the cyclooxygenase synthase inhibitor indomethacin, nor the selective thromboxane A2/prostaglandin H2 receptor antagonist SQ29,548 had any effect on angiotensin II AT1-receptor antagonist-stimulated NO release in platelets and endothelial cells. The presented studies clearly indicate a crucial role of NO in the arterial antithrombotic effects of angiotensin II AT1-receptor antagonists.
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Free combination hypertension medication is associated with a lower compliance and less persistence compared to fixed combination therapy and can, therefore, be associated with insufficient blood pressure reductions. This non-randomized study investigated whether valsartan 160 mg/hydrochlorothiazide 25 mg (Val 160/HCTZ 25) in fixed dose combination could provide additional blood pressure control in hypertensive patients not adequately controlled by the free combination of candesartan 32 mg plus HCTZ 25 mg.
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Our results suggest that AII is a potent mitogen for SMCs of ophthalmic arteries, an effect that is enhanced in the presence of insulin, and that it may be an important contributor to structural vascular changes in the ophthalmic circulation in hypertension associated with non-insulin dependent diabetes. The inhibition of AII-induced growth by an AT1 antagonist suggests that these drugs may be important therapeutic tools to prevent structural vascular changes in the ophthalmic vasculature under these conditions.
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The efficacy and tolerability of eplerenone, a selective aldosterone blocker, was assessed when added to existing antihypertensive therapy with an ACE inhibitor or an angiotensin II receptor blocker (ARB). Hypertensive patients (n=341) whose blood pressure (BP) was not controlled despite ACE inhibitor or ARB were randomized (double-blind) to receive 50 mg eplerenone (increasing to 100 mg if required) once daily or placebo for 8 weeks. Diastolic and systolic BP and adverse events were recorded. By study end (week 8), mean seated diastolic BP was significantly reduced from week 0 among patients receiving eplerenone/ARB (-12.7+/-0.81 mm Hg) compared with those receiving placebo/ARB (-9.3+/-0.83 mm Hg). The change in mean seated diastolic BP was -9.9+/-0.88 mm Hg in eplerenone/ACE inhibitor patients and -8.0+/-0.86 mm Hg in placebo/ACE inhibitor patients (P=NS). Systolic BP levels were also significantly lower at week 8 for eplerenone/ACE inhibitor (-13.4+/-1.35 mm Hg) and eplerenone/ARB (-16.0+/-1.37 mm Hg) patients, respectively, compared with placebo/ACE inhibitor (-7.5+/-1.31 mm Hg) and placebo/ARB patients (-9.2+/-1.41 mm Hg). Adverse events were generally nonsevere and not significantly different between eplerenone and placebo. This study demonstrated that in patients whose BP was not controlled with an ACE inhibitor or ARB, the addition of eplerenone over an 8-week period significantly lowered systolic BP in both groups and diastolic BP in ARB patients. Selective aldosterone blockade with eplerenone, therefore, may be useful add-on therapy in hypertensive patients inadequately controlled on ACE inhibitor or ARB alone.