br Eprosartan The AT R antagonist eprosartan is approved for

Eprosartan The AT1R antagonist eprosartan is approved for the treatment of essential Fmoc-Asp-OAll mg and may be administered using a convenient once-daily regimen. The drug is a well-tolerated and effective antihypertensive agent with benefit in the secondary prevention of cerebrovascular events, independent of BP-lowering effects. Eprosartan has a low potential for serious adverse events and has not been associated with clinically significant drug interactions, establishing it as a promising agent for combination antihypertensive strategies. Accordingly, eprosartan represents a useful therapeutic option in the management of patients with hypertension, including those who have had a stroke and those with co-morbid type 2 DM [29]. Eprosartan therapy caused positive changes in the indicators of vascular-thrombocytic (diminished platelet aggregation, reduced surplus of von Willebrand factor and endothelin-1) and secondary (decreased coagulation factor VII activity, longer activated partial thromboplastin time) hemostasis and the anticoagulant (reduced antithrombin III deficiency) and fibrinolytic (elevated blood plasminogen concentrations) systems, suggesting that the pleiotropic effects of eprosartan may be used to correct hypercoagulability syndrome in patients with chronic kidney disease associated with hereditary thrombophilia [30]. Use of eprosartan-based treatment for one year was associated with sustained reduction in BP and stabilization or improvement of mini mental state examination scores [31]. Because eprosartan is more effective in inhibiting sympathetic nervous system activity compared to other chemically distinct nonpeptide AT1R antagonists, eprosartan may be more effective in lowering systolic BP and in treating isolated systolic hypertension [32].
Comparison There are several advantages and drawbacks as well for each ARB and thus a comparison of them would provide some good idea for their selection during a particular therapy. Cost-effectiveness analysis shows that treatment of mild arterial hypertension with olmesartan is more appropriate from the pharmacoeconomic point of view than losartan and valsartan, both in general group and in patients with DM and renal failure [33]. The B2R agonistic property of losartan can confer additional beneficial effects and may be considered superior to other ARBs in the treatment HF patients. In animal models of hypertension and diabetic nephropathy, azilsartan medoxomil was shown to be a long-lasting and orally active AT1R blocker, and its antihypertensive, insulin-sensitising and antiproteinuric effects were superior to those of olmesartan medoxomil and thereby suggesting that azilsartan medoxomil could be a valuable AT1R blocker for treatment of hypertensive patients [34]. In cultured 3T3-L1 preadipocytes, azilsartan enhanced adipogenesis and exerted greater effects than valsartan on expression of genes encoding 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 Ang II. In aortic endothelial cells, azilsartan inhibited cell proliferation at concentrations as low as 1μmol/L, whereas valsartan showed little or no antiproliferative effects at concentrations below 10μmol/L. Antiproliferative effects of azilsartan were also observed in cells lacking AT1R. In addition, azilsartan, but not valsartan, blocked Ang II-induced activation of MAPK in vascular smooth muscle cells 4–8h after washout of drug from the incubation media [35]. Compared to the maximum doses of three other ARBs (valsartan, olmesartan, and candesartan), azilsartan appears to be more efficacious in reducing BP, with a similar safety and tolerability profile. Once-daily azilsartan medoxomil effectively lowers BP in adults with essential hypertension and has shown better antihypertensive efficacy than maximum therapeutic dosages of olmesartan medoxomil or valsartan in major trials of up to 24 weeks׳ duration [24]. Based on these reports, we can suggest that, azilsartan is better than candesartan, olmesartan and valsartan; losartan is better than eprosartan and valsartan; fimasartan is better than losartan and valsartan; olmesartan is better than losartan, valsartan and irbesartan; telmisartan is superior to losartan; valsartan produced better LV hypertrophy reduction than losartan (Supplementary table).