Bisoprolol, carvedilol, enalapril are widely used for the treatment of patients with chronic heart failure. Definite role in the treatment of these patients is also played by angiotensin-II receptor blockers. Diastolic left ventricular function is widely spread among patients with chronic heart failure and its important value for prognosis has been demonstrated. However effect of modern drugs used for the treatment of chronic heart failure has been poorly studied. We assessed effects of enalapril, its combination with bisoprolol, carvedilol, and irbesartan on parameters of diastolic function in a randomized prospective controlled study on 84 patients with NYHA class III-IV heart failure and left ventricular ejection fraction <40%. It has been shown that left ventricular dysfunction is highly prevalent in patients with chronic heart failure and that differentiated approach to the choice of a drug for the treatment of chronic heart failure requires consideration of the type of diastolic dysfunction.
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Angiotensin (Ang) II type 2 (AT(2)) receptors are believed to counteract Ang II type 1 (AT(1)) receptor-mediated effects. Here, we investigated AT(2) receptor-mediated effects on coronary and cardiac contractility in C57BL/6 mice. Hearts were perfused according to Langendorff. Baseline coronary flow (CF) and left ventricular systolic pressure (LVSP) were 2.7 +/- 0.1 ml min(-1) and 111 +/- 3 mmHg (n = 50), respectively. Ang II (n = 14) concentration dependently decreased CF and LVSP, by maximally 41 +/- 4 and 25 +/- 3%, respectively (pEC(50)s 7.41 +/- 0.12 and 7.65 +/- 0.12). The AT(1) receptor antagonist irbesartan (n = 4) abolished all Ang II-induced changes, whereas the AT(2) receptor antagonist PD123319 (n = 6) enhanced (P < 0.05) the effect of Ang II on CF (to 59 +/- 1%) and LVSP (to 44 +/- 2%), without altering its potency. A similar enhancement was observed in the presence of nitric oxide (NO) synthase inhibitor N(omega)-nitro-L-arginine methyl ester HCl (L-NAME; n = 4). On top of L-NAME, PD123319 no longer affected the response to Ang II (n = 4). The AT(2) receptor agonist CGP42112A (n = 4) did not affect CF or LVSP, nor did CGP42112A (n = 4) alter the constrictor response to the alpha(1)-adrenoceptor agonist phenylephrine. Furthermore, Ang II exerted no effects in hearts of AT(1A)(-/-) mice (n = 5), whereas its effects in hearts of AT(1A)(+/+) wild-type control mice (n = 7) were indistinguishable from those in hearts of C57BL/6 mice. In conclusion, Ang II exerts opposite effects on coronary and cardiac contractility in the mouse heart via activation of AT(1A) and AT(2) receptors. AT(2) receptor-mediated effects depend on NO and occur only in conjunction with AT(1A) receptor activation.
Olmesartan medoxomil is a competitively priced addition to the class of angiotensin II receptor antagonists. Monotherapy with olmesartan medoxomil in once-daily doses of 20-40 mg has produced significant reductions in systolic and diastolic blood pressure in hypertensive patients. Adverse effects have been minimal with olmesartan medoxomil, with dizziness being the only adverse effect occurring more often than with placebo in clinical trials. Additionally, animal studies indicate that olmesartan medoxomil may prove to be useful treatment for diabetic nephropathy, as well as atherosclerosis.
Shenkangwan and irbesartan reduced the urinary protein quantity in 24 h and alleviated the renal damage in DN rats, and the expression of desmin was significantly attenuated while podocin expression increased in the podocytes.
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Specific features of the 24-h blood pressure (BP) pattern are linked to progressive injury of target tissues and risk of cardiovascular disease (CVD) events. Several studies have consistently shown an association between blunted asleep BP decline and risk of fatal and nonfatal CVD events. Thus, there is growing focus on ways to properly control BP during nighttime sleep as well as during daytime activity. One strategy, termed chronotherapy, entails the timing of hypertension medications to endogenous circadian rhythm determinants of the 24-h BP pattern. Significant and clinically meaningful treatment-time differences in the beneficial and/or adverse effects of at least six different classes of hypertension medications, and their combinations, are now known. Generally, calcium channel blockers (CCBs) are more effective with bedtime than morning dosing, and for dihydropyridine derivatives bedtime dosing significantly reduces risk of peripheral edema. The renin-angiotensin-aldosterone system is highly circadian rhythmic and activates during nighttime sleep. Accordingly, evening/bedtime ingestion of the angiotensin-converting enzyme inhibitors (ACEIs) benazepril, captopril, enalapril, lisinopril, perindopril, quinapril, ramipril, spirapril, trandolapril, and zofenopril exerts more marked effect on the asleep than awake systolic (SBP) and diastolic (DBP) BP means. Likewise, the bedtime, in comparison with morning, ingestion schedule of the angiotensin-II receptor blockers (ARBs irbesartan, olmesartan, telmisartan, and valsartan exerts greater therapeutic effect on asleep BP, plus significant increase in the sleep-time relative BP decline, with the additional benefit, independent of drug terminal half-life, of converting the 24-h BP profile into a more normal dipping pattern. This is the case also for the bedtime versus upon-awakening regimen of combination ARB-CCB, ACEI-CCB, and ARB-diuretic medications. The chronotherapy of conventional hypertension medications constitutes a new and cost-effective strategy for enhancing the control of daytime and nighttime SBP and DBP levels, normalizing the dipping status of their 24-h patterning, and potentially reducing the risk of CVD events and end-organ injury, for example, of the blood vessels and tissues of the heart, brain, kidney, and retina.
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Early use of ARB/HCTZ combination therapy achieves critical decrease in BP and is an effective treatment for patients with moderate to severe HTN. Angiotensin receptor blockers also have renal- and CV-protective properties in conjunction with their antihypertensive effects, providing additional benefit to patients who at risk of vascular disease.
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Sixty-four microalbuminuric hypertensive (group 1) and 60 microalbuminuric normotensive (group 2) type 2 diabetic male patients, matched for age, BMI, HbA(1c), and diabetes duration, were enrolled. Each group was divided into two subgroups receiving either irbesartan (150 mg b.i.d. orally) or placebo for 60 days. After 15 days of washout, irbesartan was given to the subgroups who had received the placebo, and vice versa, in a randomized double-blind crossover study.
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A total of 200 patients were randomised to irbesartan 75 mg or enalapril 10 mg (once daily). Doses were doubled at Weeks 4 and/or 8 if seated diastolic blood pressure (DBP) was > or = 90 mm Hg. Trough blood pressure was measured after completion of a 4- to 5-week placebo lead-in period and again after 2, 4, 8, and 12 weeks of treatment.
Evidence is currently equivocal on the added benefits of dual blockade of the renin-angiotensin-aldosterone system with the combination of either an ACE inhibitor (ACEI) plus an angiotensin II type 1 receptor antagonist (angiotensin receptor blocker [ARB]) or aliskiren, the first-in-class direct renin inhibitor, plus an ARB.
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Osteoprotegerin (OPG) is a secreted member of the tumor necrosis factor receptor family, and in previous studies has been shown to regulate osteoclast activity and differentiation. Ablation of the OPG gene in mice results in calcification of the aorta and renal arteries. We have previously reported an association between a single nucleotide polymorphism in the promoter region of OPG and vascular morphology and function in healthy humans. The objective with this study was to confirm our previous results in a larger population, and in addition, to study subjects with hypertension. The OPG genotype was determined by restriction fragment length and the intima-media thickness (IMT) of the common carotid artery was measured by ultrasound in 100 patients with hypertension and left ventricular hypertrophy, and 75 healthy normotensive control subjects. In the hypertensive group subjects with the CC genotype (n=24) showed a significantly increased IMT compared to those with the TC (n=52, p=0.007) and TT (n=24, p=0.009) genotype, in the hypertensive group only (mean +/- SD for TT=0.88 +/- 0.21 mm, TC=0.90 +/- 0.16 mm, CC=1.05 +/- 0.31 mm). The allele distribution did not differ between hypertensive and control individuals. The present study confirms our previous finding and shows that polymorphism in the promoter region of OPG is associated with vascular morphology in hypertensive subjects.
Large and small arteries are remodelled in hypertension - their structure, function and mechanics are altered. These changes contribute to elevated blood pressure and to the complications of hypertension. The present paper concentrates on small (resistance) artery changes in hypertension. In hypertension, these vessels exhibit a form of remodelling known as 'eutrophic' remodelling, in which smooth muscle cells are restructured around a smaller lumen, without true hypertrophy, particularly in milder forms of hypertension. Changes in these small arteries are the first manifestation of target organ damage in patients with hypertension. In more severe forms of hypertension and in secondary hypertension, hypertrophic remodelling has been reported. Stiffness of the vessel wall may be decreased initially; later, as hypertension becomes more severe, the wall of resistance vessels may become stiffer. Endothelial dysfunction occurs in a percentage of patients, similar to the prevalence of left ventricular hypertrophy. Interruption of the renin-angiotensin system may correct many of these abnormalities. The present report investigated the effects of angiotensin type 1 (AT1) receptor antagonists on small arteries of hypertensive patients compared with the beta-blocker atenolol in different studies. Beta-blocker treatment did not modify either the structure or the function of small arteries in contrast to the AT1 antagonist losartan in a double-blind, randomized, one-year study. Patients previously treated with atenolol to lower blood pressure, but whose small artery structure and function did not improve, were examined. These hypertensive patients were switched to the AT1 antagonist irbesartan for one year. Gluteal subcutaneous biopsies showed that the structure and endothelial function of small arteries that had remained altered by atenolol treatment were corrected by irbesartan treatment, although blood pressure control with irbesartan was identical to that previously achieved with atenolol. Improved outcomes in clinical trials using angiotensin-converting enzyme inhibitors and AT1 receptor antagonists may be a result of the vascular protective effects offered by these agents.
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At 90 minutes after capsule administration, only losartan did not significantly reduce ΔSBP in response to the 3 higher angiotensin doses, compared with placebo. Among drug treatments, telmisartan (3 mg/kg dosage) attenuated ΔSBP to a significantly greater degree than benazepril and all other treatments. At 24 hours, telmisartan was more effective than benazepril (mean ± SEM ΔSBP, 15.7 ± 1.9 mm Hg vs 55.9 ± 12.42 mm Hg, respectively).
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PRA was high prior to drug administration, indicating slight salt depletion, and dropped by 65% after intake of celecoxib alone (p = 0.008) but only by 25% after combined intake with irbesartan (p = n.s.). GFR was not affected either by celecoxib alone or by combined administration with irbesartan. In contrast, ERPF increased by 28% 80 minutes after simultaneous drug intake (p = 0.029), but not after celecoxib alone. Renal sodium and potassium excretion did not significantly change under celecoxib alone or in combination with irbesartan.
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To observe the effect of acupuncture on cationized bovine serum albumin (C-BSA) nephritis model in rabbits and to explore its mechanism.
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The purpose of this study was to assess the safety and antihypertensive dose-response effects of irbesartan and hydrochlorothiazide (HCTZ) in patients with mild-to-moderate hypertension. After a 4- to 5-week single-blind placebo lead-in period, 683 patients with seated diastolic blood pressure (SeDBP) between 95 and 110 mm Hg were randomized to receive once-daily dosing with one of 16 different double-blind, fixed combinations of irbesartan (0, 37.5, 100, and 300 mg irbesartan) and HCTZ (0, 6.25, 12.5, and 25 mg HCTZ) for 8 weeks. The primary efficacy variable was the change from baseline in trough SeDBP after 8 weeks of therapy. Data were analyzed by response surface modeling. At Week 8, mean changes from baseline in trough SeDBP (mm Hg) ranged from -3.5 for placebo, -7.1 to -10.2 for the irbesartan monotherapy groups, -5.1 to -8.3 for the HCTZ monotherapy groups, and -8.1 to -15.0 for the combination groups. Irbesartan plus HCTZ produced additive reductions in both SeDBP and seated systolic BP, with at least one combination producing greater BP reduction than either drug alone (P < .001). All treatments were well tolerated; there were no treatment-related serious adverse events. Irbesartan tended to ameliorate the dose-related biochemical abnormalities associated with HCTZ alone. In conclusion, the combination of HCTZ in doses up to 25 mg with irbesartan, in doses up to 300 mg, is safe and produces dose-dependent reductions in BP.
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Two studies comparing the cost-effectiveness of irbesartan to similar blood pressure control with standard antihypertensive medications (excluding angiotensin-converting enzyme inhibitors and other angiotensin receptor blockers) in treatment of patients with hypertension, type 2 diabetes, and microalbuminuria have been published to date; one in a United States setting, the other in a Spanish setting. Both studies were based on a Markov-based Monte Carlo simulation model, with the effects of irbesartan or standard blood pressure control taken from the Irbesartan Reduction of Microalbuminuria-2 (IRMA-2) and the Irbesartan in Diabetic Nephropathy Trial (IDNT) clinical trials. In both Spanish and U.S. settings, irbesartan was projected to delay the onset of end-stage renal disease (ESRD), reduce the cumulative incidence of ESRD, increase life expectancy, and reduce overall direct medical costs. Irbesartan treatment of patients with type 2 diabetes, hypertension, and microalbuminuria may lead to major improvements in long-term patient outcomes, with substantial cost savings as an added bonus to third party payers.
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The association of bioactive nucleus with other pharmacological agents is hoped to improve the efficacy of the treatment by combining the effects of different pharmacological mechanisms of action. Keeping this in view, a series of 2-butyl-1,3-diaza-spiro[4,4]non-1-en-4-one derivatives have been synthesized by interaction of 2-butyl-1,3-diaza-spiro[4,4]non-1-en-4-one with different bioactive aralkyl halides in presence of powdered potassium carbonate by two different methods viz., conventional and microwave irradiation. The yields under conventional and microwave irradiation methods were in the range of 60-65% and 80-90%, respectively. The structure elucidation of the new compounds has been carried out with the help of elemental analysis and spectral data. All the synthesized compounds have been screened for their efficacy as acetylcholinesterase (AChE) inhibitor. AChE inhibitory activity study was carried out by using Ellman colorimetric assay with neostigmine as a reference standard against targets from different species, such as pure electric eel AChE, human serum AChE, and rat brain AChE. Among the compounds synthesized, compounds 5a, 5b, 5j showed good inhibition against AChE.
Atrial fibrillation (AFib) is common in heart failure (HF) with preserved ejection fraction (HFpEF). Current AFib stroke risk prediction models include the presence of HF but do not specifically include HFpEF as a risk factor. Whether a history of AFib should be used to identify patients with HFpEF who are at risk has not been established.
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Focal brain ischemia resulted in a strong induction of c-Fos and c-Jun proteins in the cortex, which positively correlated with the degree of neurological deficits. Treatment of rats with irbesartan significantly improved neurological outcome of focal cerebral ischemia when compared with the vehicle-treated group and markedly reduced the expression of c-Fos and c-Jun proteins in the cortex on the ligated side of the brain. Irbesartan pretreatment completely abolished the ischemia-induced c-Fos expression in the hippocampus.
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Hemodynamic and non-hemodynamic factors contribute to the development of left ventricular hypertrophy (LVH). The presence of LVH is an important independent risk factor for total mortality and for cardiovascular morbidity and mortality. Direct cardiac effects of LVH include an increased risk of developing of congestive heart failure, an increased risk of arrhythmic events, and a reduced coronary flow reserve, promoting myocardial ischemic episodes. In addition, hypertension may promote the development of coronary artery atherosclerosis. The prognostic implications of LVH underscore the importance of diagnostic procedures. The electrocardiogram has a high specificity to identify patients with LVH but the sensitivity is fairly low. Echocardiography provides higher sensitivity and also gives important information, such as the pattern of left ventricular geometry, which is of prognostic importance, and the presence of diastolic dysfunction, which is an early abnormality in the evolution of hypertensive LVH. Reversal of LVH appears to improve prognosis. Reduction of blood pressure is one important component in the regression of LVH. Important quantitative differences exist between drug classes in the reversal of cardiac hypertrophy despite similar antihypertensive effects, suggesting other factors to be of importance in the regression of left ventricular mass. LVH is reduced more by angiotensin-converting enzyme inhibitors than by other antihypertensive drug classes, suggesting an effect on structural myocardial changes beyond that provided by the reduction of blood pressure. Recent data suggest that angiotensin II receptor antagonists (AIIRAs) have quantitatively similar effects on left ventricular mass as do angiotensin-converting enzyme inhibitors. A comparative trial of the AIIRA irbesartan and the beta-blocker atenolol demonstrated that despite similar reductions in blood pressure, the reductions attained in left ventricular mass with irbesartan were progressive and numerically greater than those attained with atenolol. Taken together, these findings provide circumstantial evidence for an important role of angiotensin II acting on angiotensin type 1 (AT1) receptors in the development or maintenance of cardiac hypertrophy. Confirmation of the favorable effects of angiotensin-converting enzyme inhibitors and AIIRAs on left ventricular mass in larger trials, including those assessing cardiovascular morbidity and mortality, will be of major importance in the future treatment of hypertension.
Pigment epithelium-derived factor (PEDF), a serine protease inhibitor, regulates extracellular matrix production in the kidney. We sought the association between urinary PEDF (uPEDF) and development of nephropathy among patients with type 2 diabetes (T2DM).
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Haemodynamic function, circulating renin-angiotensin system mediators and norepinephrine were measured in young healthy subjects at baseline and at 2 and 4 weeks after treatment with irbesartan. Subjects were divided into two groups on the basis of the AT2R G1675A gene polymorphism: GG subjects (n = 12) and AA/GA subjects (n = 22).
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Renal protective effects in diabetic patients. Blocking the renin-angiotensin system slows the progression of nephropathy and end-stage renal disease in diabetes mellitus. While substantial evidence exists for the renal protective effects of angiotensin converting enzyme (ACE) inhibitors in patients with insulin-dependent diabetes mellitus (IDDM), the role of renin-angiotensin system blockade in non-insulin-dependent diabetes mellitus (NIDDM) is less clear. The evidence regarding ACE inhibitors has been attained through the traditional channels of evidence-based medicine: observational studies, trials in animal models, preliminary human analyses, and large, randomized trials. While a sound approach, these pathways to elucidating therapeutic effects require the expenditure of substantial time and resources. Accelerated trials with angiotensin II receptor antagonists have relied on the proven effects of ACE inhibitors in the diabetic patient, as well as on pharmacologic principles dictating that renin-angiotensin blockade is more complete when the system is interrupted at the rate-limiting or receptor level. Irbesartan and creatinine clearance in NIDDM patients. The Collaborative Study pilot trial has already shown that the angiotensin II receptor antagonist irbesartan is significantly more effective than the calcium antagonist amlodipine on creatinine clearance in hypertensive NIDDM patients. Subsequent to this trial, a large, randomized study of over 1600 hypertensive patients with NIDDM has been initiated. Other trials have indicated that the response to blocking angiotensin II receptors with irbesartan in patients with NIDDM is substantially larger than it is in healthy humans.
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Searches of MEDLINE and International Pharmaceutical Abstracts through July 2011 were conducted. Search terms used included child, pediatric, hypertension, and the following drugs: captopril, enalapril, lisinopril, fosinopril, losartan, valsartan, irbesartan, candesartan, olmesartan, amlodipine, nifedipine, isradipine, felodipine, propranolol, metoprolol, labetalol, minoxidil, furosemide, spironolactone, chlorothiazide, hydrochlorothiazide, hydralazine, and prazosin. Clinical trial data were reviewed and evaluated and were limited to English-language articles.
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A strong causal link exists between psychological stress and insulin resistance as well with hypertension. Meanwhile, stress-related responses play critical roles in glucose metabolism in hypertensive patients. As clinical trials suggest that angiotensin-receptor blocker delays the onset of diabetes in hypertensive patients, we investigated the effects of irbesartan on stress-induced adipose tissue inflammation and insulin resistance. C57BL/6J mice were subjected to 2-week intermittent restraint stress and orally treated with vehicle, 3 and 10 mg/kg/day irbesartan. The plasma concentrations of lipid and proinflammatory cytokines [Monocyte Chemoattractant Protein-1 (MCP-1), tumor necrosis factor-α, and interleukin-6] were assessed with enzyme-linked immunosorbent assay. Monocyte/macrophage accumulation in inguinal white adipose tissue (WAT) was observed with CD11b-positive cell counts and mRNA expressions of CD68 and F4/80 using immunohistochemistry and RT-PCR methods respectively. The mRNA levels of angiotensinogen, proinflammatory cytokines shown above, and adiponectin in WAT were also assessed with RT-PCR method. Glucose metabolism was assessed by glucose tolerance tests (GTTs) and insulin tolerance tests, and mRNA expression of insulin receptor substrate-1 (IRS-1) and glucose transporter 4 (GLUT4) in WAT. Restraint stress increased monocyte accumulation, plasma free fatty acids, expression of angiotensinogen and proinflammatory cytokines including MCP-1, and reduced adiponectin. Irbesartan reduced stress-induced monocyte accumulation in WAT in a dose dependent manner. Irbesartan treatment also suppressed induction of adipose angiotensinogen and proinflammatory cytokines in WAT and blood, and reversed changes in adiponectin expression. Notably, irbesartan suppressed stress-induced reduction in adipose tissue weight and free fatty acid release, and improved insulin tolerance with restoration of IRS-1 and GLUT4 mRNA expressions in WAT. The results indicate that irbesartan improves stress-induced adipose tissue inflammation and insulin resistance. Our results suggests that irbesartan treatment exerts additive benefits for glucose metabolism in hypertensive patients with mental stress.