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Goal blood pressure levels are only being achieved in approximately a third of hypertensive patients, which suggests that there is a need for new and/or improved approaches to the treatment of hypertension. The majority of patients with hypertension require combination therapy to control their blood pressure. The use of a combination of drugs with complementary mechanisms of action may provide greater efficacy and tolerability compared with monotherapy, and may allow more rapid achievement of target blood pressure. Moreover, the use of single-pill combinations has the potential to increase adherence and persistence, and reduce costs. The single-pill combination of valsartan plus hydrochlorothiazide was recently approved by the US FDA for first-line use in hypertensive patients who are likely to need multiple drugs to achieve their blood pressure goals. The focus of this article is on those randomized, double-blind trials in which this combination was administered as first-line therapy in patients with essential hypertension.
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Molecular modeling has proven valuable to generate testable hypotheses concerning receptor/ligand binding and is an important tool in drug design. ARBs were designed to act as antagonists for AT2R1, and it was not surprising to discover their affinity for the structurally similar CCR2b. However, this study also found evidence that ARBs modulate the activation of two key nuclear receptors-VDR and PPARgamma. If our simulations are confirmed by experiment, it is possible that ARBs may become useful as potent anti-inflammatory agents, in addition to their current indication as cardiovascular drugs.
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Triptolide can dramatically attenuate albuminuria and renal lesion accompanied with dyslipidaemia and obesity in db/db diabetic mice. It is a new drug that exerts comprehensive protective effects on preventing DN progression.
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Cholesterol crystal embolism (CCE) is a systemic disease resulting from shedding of cholesterol crystals into the small vessels of multiple organs, including skin, kidney, gastrointestinal tract and others. Recently, neuroendovascular therapeutic procedures for athrosclerosis disease is increasing. We report a case of CCE after carotid stenting (CAS). A 73-year-old man with asymptomatic carotid stenosis was treated by percutanenous transluminal angioplasty with stenting. CAS was achieved in a short time without trouble. About 1 month after CAS, his renal function deteriorated and purpura appeared on both toe tips (blue toe syndrome) with muscle pain of the lower extremities. Under diagnosis of CCE, he was treated by Predonisolone 20 mg/day and Valsartan 160 mg/day, Pravastatin 10 mg/day. His symptom's dramatically improved, with partial recovery of renal function. CCE rarely occurs after angiographic or interventional procedures, but is difficult to diagnose clinically and there is no established therapy. For early diagnosis of CCE strict follow-up of a patients clinical presentation and laboratory data, especially in high risk patients, is needed.
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We enrolled 196 patients with hypertension who were already being treated with free-drug combinations of angiotensin-II receptor blocker (ARB) and amlodipine. The free-drug combinations of ARB and amlodipine were replaced with the same dose of the fixed-dose combinations. The average home blood pressure (BP) in all patients receiving fixed-dose combinations was significantly lower than those receiving free-drug combinations (131 ± 10/75 ± 8 vs. 136 ± 11/77 ± 9 mm Hg, P < .01) accompanied with increasing drug adherence. After lowering BP by fixed-dose combinations, the costs for medications decreased by 31% over the 3 months.
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Although valsartan decreased plasma ET-1 in these mice, it did not affect ET(A) or ET(B) in their kidneys. Co-treatment with valsartan and bosentan decreased ET-1 in these mice compared to the single treatments. Bosentan, but not valsartan, elevated eNOS expression in their kidneys. Co-treatment with valsartan and bosentan reduced TGF-β, α-SMA, and collagen IV expression, and the Masson's trichrome stained area in their kidneys.
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p27(kip1), p21(cip1) protein expression in podocytes exposed to high glucose for 72 h and in 16 weeks diabetic glomeruli significantly increased (P<0.01). The expressions of bax, cleaved caspase-3 increased while the expression of bcl-2 decreased in diabetic glomeruli as well as in high glucose. But they were all ameliorated in the groups treated with either MMF or Valsartan.
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Eight weeks after procedure, hypertension rats developed significantly cardiac hypertrophy, and the protein expression of Calpain I, mRNA and protein expression and the activity of calcineurin were significantly increased compared sham-operated control rats (all P<0.01), the mRNA expression of CaMKIIδA and B increased, CaMKIIδC mRNA decreased (P<0.01). Treatment with valsartan effectively attenuated cardiac hypertrophy and reversed hypertension induced changes on myocardial Calpain I, calcineurin and CaMKIIδ.
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Non-alcoholic fatty liver disease (NAFLD) is associated with features of the metabolic syndrome (MetS) and may be an expression of the syndrome within the liver. Using screening data from the Nateglinide And Valsartan in Impaired Glucose Tolerance Outcomes Research (NAVIGATOR) study (n = 42 149), we examined whether alanine aminotransferase (ALT), a biomarker for NAFLD, clustered with features of MetS and whether the clusters differed across global geographic regions.
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We performed ambulatory BP monitoring before and after once-daily dose of valsartan (valsartan group, n = 38) and amlodipine (amlodipine group, n = 38) therapy in 76 hypertensive patients. To achieve the target BP of < or =140/90 mm Hg, valsartan was titrated from 40 mg/day to 160 mg/day (mean dose 124 mg/day) and amlodipine was titrated from 2.5 mg/day to 10 mg/day (mean dose 6.4 mg/day).
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Our findings implicate that local renin angiotensin system activation in podocytes is partly involved in down-regulation of nephrin by mesangial medium in IgA nephropathy.
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Amlodipine, a dihydropyridine calcium channel blocker, and valsartan, an angiotensin II receptor blocker, are co-formulated in a single-dose combination for the treatment of hypertension. The combination is used by patients whose blood pressure is not adequately controlled on either component monotherapy. This work describes a simple, sensitive, and reliable spectrofluorimetric method for the simultaneous determination of the two antihypertensive drugs; amlodipine besylate (AML) and valsartan (VAL) in their combined tablets. The method involved measurement of the native fluorescence at 455 nm (λ(Ex) 360 nm) and 378 nm (λ(Ex) 245 nm) for AML and VAL, respectively. Analytical performance of the proposed spectrofluorimetric procedure was statistically validated with respect to linearity, ranges, precision, accuracy, selectivity, robustness, detection, and quantification limits. Regression analysis showed good correlation between fluorescence intensity and concentration over the concentration ranges 0.2-3.6 and 0.008-0.080 µg mL⁻¹ for AML and VAL, respectively. The limits of detection were 0.025 and 0.0012 µg mL⁻¹ for AML and VAL, respectively. The proposed method was successfully applied for the assay of the two drugs in their combined pharmaceutical tablets with recoveries not less than 98.85%. No interference was observed from common pharmaceutical additives. The results were favourably compared with those obtained by a reference spectrophotometric method.
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Type 2 diabetes mellitus is becoming a major health problem associated with excess morbidity and mortality. As the prevalence of type 2 diabetes is rapidly increasing, prevention of the disease should be considered as a key objective in the near future. Besides lifestyle changes, various pharmacological treatments have proven their efficacy in placebo-controlled clinical trials, including antidiabetic drugs such as metformin, acarbose and troglitazone, or antiobesity agents such as orlistat. Arterial hypertension, a clinical entity in which insulin resistance is common, is strongly associated with type 2 diabetes and may precede the disease by several years. While antihypertensive agents such as diuretics or beta-adrenoceptor antagonists may worsen insulin resistance and impair glucose tolerance, newer antihypertensive agents exert neutral or even slightly positive metabolic effects. Numerous clinical trials have investigated the effects of ACE inhibitors or angiotensin II receptor antagonists (ARAs) on insulin sensitivity in hypertensive patients, with or without diabetes, with no consistent results. Almost half of the studies with ACE inhibitors in hypertensive nondiabetic individuals demonstrated a slight but significant increase in insulin sensitivity as assessed by insulin-stimulated glucose disposal during a euglycaemic hyperinsulinaemic clamp, while the other half failed to reveal any significant change. The effects of ARAs on insulin sensitivity are neutral in most studies. Mechanisms of improvement of glucose tolerance and insulin sensitivity through the inhibition of the renin-angiotensin system (RAS) are complex. They may include improvement of blood flow and microcirculation in skeletal muscles and, thereby, enhancement of insulin and glucose delivery to the insulin-sensitive tissues, facilitating insulin signalling at the cellular level and improvement of insulin secretion by the beta cells. Six recent large-scale clinical studies reported a remarkably consistent reduction in the incidence of type 2 diabetes in hypertensive patients treated with either ACE inhibitors or ARAs for 3-6 years, compared with a thiazide diuretic, beta-adrenoceptor antagonist, the calcium channel antagonist amlodipine or even placebo. The relative risk reduction averaged 14% (p = 0.034) in the CAPPP (Captopril Prevention Project) with captopril compared with a thiazide or beta1-adrenoceptor antagonist, 34% (p < 0.001) in the HOPE (Heart Outcomes Prevention Evaluation) study with ramipril compared with placebo, 30% (p < 0.001) in the ALLHAT (Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial) with lisinopril compared with chlortalidone, 25% (p < 0.001) in the LIFE (Losartan Intervention For Endpoint reduction in hypertension study) with losartan compared with atenolol, and 25% (p = 0.09) in the SCOPE (Study on Cognition and Prognosis in the Elderly) with candesartan cilexetil compared with placebo, and 23% (p < 0.0001) in the VALUE (Valsartan Antihypertensive Long-term Use Evaluation) trial with valsartan compared with amlodipine. All these studies considered the development of diabetes as a secondary endpoint, except the HOPE trial where it was a post hoc analysis. These encouraging observations led to the initiation of two large, prospective, placebo-controlled randomised clinical trials whose primary outcome is the prevention of type 2 diabetes: the DREAM (Diabetes REduction Approaches with ramipril and rosiglitazone Medications) trial with the ACE inhibitor ramipril and the NAVIGATOR (Nateglinide And Valsartan in Impaired Glucose Tolerance Outcomes Research) trial with the ARA valsartan. Finally, ONTARGET (ONgoing Telmisartan Alone and in combination with Ramipril Global Endpoint Trial) will also investigate as a secondary endpoint whether it is possible to prevent the development of type 2 diabetes by blocking the RAS with either an ACE inhibitor or an ARA or a combination of both. Thus, the recent consistent observations of a 14-34% reduction of the development of diabetes in hypertensive patients receiving ACE inhibitors or ARAs are exciting. From a theoretical point of view, they emphasise that there are many aspects of the pathogenesis, prevention and treatment of type 2 diabetes that still need to be uncovered. From a practical point of view, they may offer a new strategy to reduce the ongoing epidemic and burden of type 2 diabetes.
VALNORM was designed to assess the impact on blood pressure (BP) control of a specific training in new European Society of Hypertension-International Society of Hypertension (ESH-ISH) guidelines for hypertension management. It was an 8-week prospective, randomized, open, blinded end points design study. General practitioners (GPs) located in France were randomized in two groups: group 1 (G1) without training to the guidelines and free attitude for the prescription whereas group 2 (G2) received a specific training in ESH guidelines. The primary efficacy criteria was strict BP control at week 8 (systolic BP/diastolic BP [SBP/DBP] <140/90 mm Hg and/or SBP/DBP <130/80 mm Hg if diabetes or renal insufficiency). All physicians used the same treatment (valsartan 80 or 160 mg once daily alone or in fixed combination with hydrochlorothiazide 12.5 or 25 mg once daily). BP was measured in the GPs' office with an electronic device. The groups GPs included 4,436 patients with essential uncontrolled hypertension (G1: 595 physicians, 2,308 patients; G2: 502 physicians, 2,128 patients). Patients' main characteristics were: age = 61 +/- 13 years, 52% female, BP = 160 +/- 13/92 +/- 9 mm Hg. No difference was observed between the two groups. The primary efficacy criteria showed in G2: 47.8% of BP control vs. G1: 44.7%, P = .005. Subgroup analysis according to age, body mass index (BMI), previous diabetes, and antihypertensive treatment showed that higher efficacy in G2 was more significant in these high-risk subgroups: age >60 years (G1: n = 1,150, G2: n = 1,035), BMI >/=25 kg/m(2) (G1: n = 1540, G2: n = 1430), diabetes (G1: n = 267, G2: n = 290), no previous antihypertensive treatment (G1: n = 1,111, G2: n = 1,005). The percentage of patients with controlled BP in each subgroup was: diabetes: G1 11.2% vs. G2 17.9% (P = .001), age >60 years: G1 40.3% vs. G2 43.7% (P = .022), BMI >/=25 kg/m(2): G1 43.2% vs. G2 45% (P = .165), untreated: G1 48.2% vs. G2 52.4% (P = .005). Specific training on the guidelines showed a positive impact on BP control, highly significant in patients at high cardiovascular risk such as diabetic hypertensive patients.
Although angiotensin (Ang) II is known to regulate renal proximal transport in a biphasic way, the receptor subtype(s) mediating these Ang II effects remained to be established. To clarify this issue, we compared the effects of Ang II in wild-type mice (WT) and Ang II type 1A receptor-deficient mice (AT(1A) KO). The Na+-HCO3- cotransporter (NBC) activity, analyzed in isolated nonperfused tubules with a fluorescent probe, was stimulated by 10(-10) mol/L Ang II but was inhibited by 10(-6) mol/L Ang II in WT. Although valsartan (AT1 antagonist) blocked both stimulation and inhibition by Ang II, PD 123,319 (AT2 antagonist) did not modify these effects of Ang II. In AT1A KO, in contrast, this biphasic regulation was lost, and only stimulation of NBC activity by 10(-6) mol/L Ang II was observed. This stimulation was blocked by valsartan but not by PD 123,319. More than 10(-8) mol/L Ang II induced a transient increase in cell Ca2+ concentrations in WT, which was again blocked by valsartan but not by PD 123,319. However, up to 10(-5) mol/L Ang II did not increase cell Ca2+ concentrations in AT1A KO. Finally, the addition of arachidonic acid inhibited the NBC activity similarly in WT and AT(1A) KO, suggesting that the inhibitory pathway involving P-450 metabolites is preserved in AT(1A) KO. These results indicate that AT(1A) mediates the biphasic regulation of NBC. Although low-level expression of AT(1B) could be responsible for the stimulation by 10(-6) mol/L Ang II in AT1A KO, no evidence was obtained for AT2 involvement.
The renin-angiotensin system (RAS) mediates proapoptotic, profibrotic, and proinflammatory processes in maladaptive conditions. Activation after myocardial infarction may initialize and promote cardiac remodeling. Using a novel positron-emitting ligand, we sought to determine the presence and time course of regional myocardial upregulation of the angiotensin II type 1 receptor (AT1R) and the blocking efficacy of various anti-RAS agents.
Angiotensin II AT1 receptor antagonists (AIIRAs) have demonstrated efficacy similar to other classes of antihypertensive agents as well as "placebo-level" tolerability at all doses. Pharmacokinetic and pharmacodynamic studies provide a framework for understanding important intra-class dissimilarities. Disparity in antagonistic effects may be determined by in vivo responses to challenges of exogenous angiotensin II (Ang II) and by ex vivo/in vitro responses to a drug's biological activity by radioligand receptor assay (RRA). Two independent studies have been conducted in which irbesartan exhibited a more pronounced and longer-lasting antagonism to the effects of exogenous Ang II than losartan and valsartan. Comparative trials have indicated that both irbesartan and candesartan show greater clinical efficacy in lowering blood pressure than losartan. Recently, we have compared the Ang II antagonistic properties of irbesartan 150 mg/day and candesartan 8 mg/day. Both drugs block AT1 receptors with "insurmountable" antagonism and demonstrate a long duration of action. While both irbesartan and candesartan showed a similar degree of antagonistic activity in vivo, distinctly higher antagonistic activity in plasma was found for irbesartan by RRA at all time-points. Furthermore, plasma renin activity during periods with high antagonistic activity was significantly higher, and aldosterone levels following Ang II stimulation were blunted to a greater extent, following administration of irbesartan. In summary, in the doses tested, irbesartan exhibits the strongest antagonism when compared with losartan, valsartan and candesartan. This finding may have clinical implications.
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Efficacy of blood pressure (BP) lowering may differ between clinical trials and what is observed in clinical practice. These differences may contribute to poor BP control rates among those at risk.
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The HGF expression of Group B was significantly higher than that of Group A (10.69 +/- 0.96% vs 5.49 +/- 1.34%; P < 0.05). Group C also showed an increased HGF level (11.85 +/- 0.87%) compared with Group A (P < 0.05). The HGF level in Group D (15.58 +/- 1.06%) was significantly higer than that of both Group B and Group C (P < 0.05). The expressions of TGF-beta1 and AngII increased with the challenged time, while valsatan treatment decreased significantly the levels of both. Valsatan treatment attenuated airway injuries of asthmatic rats induced by OVA sensitization/challenge.
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Our results suggest that nanoethosomes are efficient carriers for transdermal delivery of valsartan, for the management of hypertension.
Influenza vaccination rates varied widely in patients with heart failure with reduced ejection fraction enrolled in the PARADIGM-HF trial, and vaccination was associated with reduced risk for death, although whether this association was causal cannot be determined.
The nuclear translocation of ERK might be a precondition for the inducement of c-fos expression.