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Renin-angiotensin-aldosterone System (renin-angiotensin-aldosterone + system)
Selected AbstractsThe effect of pretreatment with renin-angiotensin-aldosterone system blockers on cardioversion success and acute recurrence of atrial fibrillationINTERNATIONAL JOURNAL OF CLINICAL PRACTICE, Issue 7 2009A. Dogan Summary Background:, Renin-angiotensin-aldosterone system (RAS) may be activated during atrial fibrillation (AF). It is unclear whether RAS inhibition may facilitate cardioversion from AF and may prevent acute recurrence of AF (ARAF). We thus investigated the effect of pretreatment with RAS blockers on cardioversion success and ARAF in patients with AF scheduled for elective cardioversion. Methods:, This observational study included 356 patients with AF undergoing elective pharmacological or electrical cardioversion. Of these patients, 135 were not included based on exclusion criteria and the remaining 221 patients were divided into RAS group (n = 116, 69 male) or non-RAS group (n = 105, 58 male) based on precardioversion use of any RAS blocker. Results:, Hypertension, coronary heart disease and heart failure were more frequent in the RAS group. Cardioversion from AF was more successful in the RAS group than in the non-RAS group (%92 vs. %82, p = 0.026). The rate of ARAF was lower in RAS group compared with that in non-RAS group (17% vs. 31%, p = 0.026). In multivariate analysis, pretreatment with RAS blockers in addition to shock number and enlarged left atrium, independently predicted ARAF (OR: 0.33, 95% CI: 0.15,0.75, p = 0.008). Independent predictors of cardioversion success were shock number and left atrial dilatation, but not use of RAS blocker. Conclusion:, Precardioversion use of RAS blockers may reduce ARAF following successful cardioversion of AF, but did not improve electrical cardioversion. [source] Mechanisms of renal hyporesponsiveness to ANP in heart failureEUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 9 2003A. Charloux Abstract The atrial natriuretic peptide (ANP) plays an important role in chronic heart failure (CHF), delaying the progression of the disease. However, despite high ANP levels, natriuresis falls when CHF progresses from a compensated to a decompensated state, suggesting emergence of renal resistance to ANP. Several mechanisms have been proposed to explain renal hyporesponsiveness, including decreased renal ANP availability, down-regulation of natriuretic peptide receptors and altered ANP intracellular transduction signal. It has been demonstrated that the activity of neutral endopeptidase (NEP) is increased in CHF, and that its inhibition enhances renal cGMP production and renal sodium excretion. In vitro as well as in vivo studies have provided strong evidence of an increased degradation of intracellular cGMP by phosphodiesterase in CHF. In experimental models, ANP-dependent natriuresis is improved by phosphodiesterase inhibitors, which may arise as new therapeutic agents in CHF. Sodium-retaining systems likely contribute to renal hyporesponsiveness to ANP through different mechanisms. Among these systems, the renin-angiotensin-aldosterone system has received particular attention, as angiotensin II and ANP have renal actions at the same sites and inhibition of angiotensin-converting enzyme and angiotensin-receptor blockade improve ANP hyporesponsiveness. Less is known about the interactions between the sympathetic nervous system, endothelin or vasopressin and ANP, which may also blunt ANP-induced natriuresis. To summarize, renal hyporesponsiveness to ANP is probably multifactorial. New treatments designed to restore renal ANP efficiency should limit sodium retention in CHF patients and thus delay the progression to overt heart failure. [source] The mechanism of improved sodium homeostasis of low-dose losartan in preascitic cirrhosisHEPATOLOGY, Issue 6 2002Florence Wong 200 Elizabeth St. Renal sodium retention on standing is one aspect of the abnormal renal sodium handling in preascitic, well-compensated patients with cirrhosis. Recently, it has been shown that low doses (7.5 mg) of the angiotensin II (Ang II) receptor antagonist, losartan, can reverse renal sodium retention on high, 200-mmol sodium/d diet in these patients and restore them to sodium balance. Therefore, the effect of 7.5 mg of losartan on sodium excretion, when changing from supine to erect posture for 2 hours, was examined in 10 well-compensated patients with cirrhosis and 9 age- and sex-matched controls on the same sodium diet, under strictly controlled metabolic conditions. In contrast to control subjects, in whom sodium excretion was unaffected, single 7.5-mg doses of losartan again restored the preascitic patients with cirrhosis to sodium balance. In addition, it blunted the fall in erect posture, induced renal sodium excretion by a reduction in proximal and distal tubular reabsorption of sodium. These changes occurred without any significant changes in blood volumes, systemic and renal hemodynamics, or glomerular filtration rate (GFR) and filtered sodium load compared with controls, and despite activation of the systemic renin-angiotensin-aldosterone system, which was still within normal levels. In conclusion, the beneficial natriuretic effects of low-dose losartan on erect posture , induced sodium retention in preascitic cirrhosis supports the suggestion that the pathophysiology of sodium retention in preascites is in part caused by an intrarenal tubular effect of Ang II in that posture. [source] Aldosterone Excess or Escape: Treating Resistant HypertensionJOURNAL OF CLINICAL HYPERTENSION, Issue 5 2009Samira Ubaid-Girioli MD Aldosterone excess or "escape" can occur after treatment with medications that block the renin-angiotensin-aldosterone system or in undiagnosed primary aldosteronism. Spironolactone is thought to be an important addition to resistant hypertension (RH) treatment. In this study, resistant (RH) and controlled (CH) hypertensives and normotensive patients were submitted to echocardiography, flow-mediated vasodilation, carotid intima-media wall thickness studies, renin plasma activity, and aldosterone plasma levels and plasma and urinary sodium and potassium concentrations at baseline (pre-spironolactone phase). Subsequently, for only RH and CH groups, 25 mg/d spironolactone was added to preexisting treatments over 6 months. Afterwards, these parameters were reassessed (post-spironolactone phase). The RH and CH groups achieved reductions in blood pressure (P<.001), decreases in left ventricular hypertrophy (P<.001), improved diastolic function (Kappa index RH: 0.219 and Kappa index CH: 0.392) and increases in aldosterone concentrations (P<.05). The RH group attained improved endothelium-dependent (P<.001) and independent (P=.007) function. Optimized RH treatment with spironolactone reduces blood pressure and improves endothelial and diastolic function and left ventricular hypertrophy despite the presence of aldosterone excess or escape. [source] Secondary Hypertension: Obesity and the Metabolic SyndromeJOURNAL OF CLINICAL HYPERTENSION, Issue 7 2008Gregory M. Singer MD The epidemic of obesity in the United States and around the world is intensifying in severity and scope and has been implicated as an underlying mechanism in systemic hypertension. Obese hypertensive individuals characteristically exhibit volume congestion, relative elevation in heart rate, and high cardiac output with concomitant activation of the renin-angiotensin-aldosterone system. When the metabolic syndrome is present, insulin resistance and hyperinsulinemia may contribute to hypertension through diverse mechanisms. Blood pressure can be lowered when weight control measures are successful, using, for example, caloric restriction, aerobic exercise, weight loss drugs, or bariatric surgery. A major clinical challenge resides in converting short-term weight reduction into a sustained benefit. Pharmacotherapy for the obese hypertensive patient may require multiple agents, with an optimal regimen consisting of inhibitors of the renin-angiotensin-aldosterone system, thiazide diuretics, ,-blockers, and calcium channel blockers if needed to attain contemporary blood pressure treatment goals. [source] Evolving Treatment Options for Prevention of Cardiovascular Events in High-Risk Hypertensive PatientsJOURNAL OF CLINICAL HYPERTENSION, Issue 11 2007Prakash Deedwania MD The identification and treatment of high-risk patients for cardiovascular disease reduces the risk of morbidity and mortality. Significant risk factors for cardiovascular events in hypertensive patients over and above dyslipidemia, smoking, and obesity include coronary heart disease, peripheral arterial disease, cerebrovascular/carotid artery disease, and diabetes. Treatment options for the reduction of cardiovascular events in hypertensive patients include diuretics, ,-blockers, ,-blockers, calcium channel blockers, angiotensin-converting enzyme (ACE) inhibitors, angiotensin receptor blockers (ARBs), and aldosterone antagonists. All of these agents, in various combinations, have been found to reduce the risk of cardiovascular events, even in high-risk patients. The use of ACE inhibitors or ARBs (usually in combination with a diuretic) has proven especially effective in reducing cardiovascular events in diabetes and, although both classes of drugs target the renin-angiotensin-aldosterone system, each has a different mechanism of action. Some investigators believe that combination therapy with an ACE inhibitor and ARB, usually given with other medications, may be more effective than either agent alone with other drugs. The Ongoing Telmisartan Alone and in Combination With Ramipril Global Endpoint Trial (ONTARGET) is evaluating the cardioprotective effect of an ACE inhibitor (ramipril) plus an ARB (telmisartan) in high-risk patients. [source] Microalbuminuria: Definition, Detection, and Clinical SignificanceJOURNAL OF CLINICAL HYPERTENSION, Issue 2004Robert D. Toto MD Proteinuria is a sign of abnormal excretion of protein by the kidney but is a nonspecific term including any or all proteins excreted. In contrast, albuminuria specifically refers to an abnormal excretion rate of albumin. Microalbuminuria refers to an abnormally increased excretion rate of albumin in the urine in the range of 30,299 mg/g creatinine. It is a marker of endothelial dysfunction and increased risk for cardiovascular morbidity and mortality especially, but not exclusively, in high-risk populations such as diabetics and hypertensives. Testing for microalbuminuria is now made easy by in-office dipstick tests (semi-quantitative) and widely available laboratory testing (quantitative). Physicians should screen all diabetics for albuminuria and strongly consider screening hypertensives to identify those at higher risk for cardiovascular disease. Appropriate intervention, including use of drugs that block the renin-angiotensin-aldosterone system, may be appropriate in such cases as suggested by the American Diabetes Association and the Seventh Report of Joint National Committee on the Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. [source] Target-organ protection with combination renin-angiotensin-system blockadeCLINICAL CARDIOLOGY, Issue 1 2009L. Michael PrisantMD FACC Abstract Pharmacologic blockade of the renin-angiotensin-aldosterone system (RAS) has antihypertensive, anti-atherogenic, antioxidant, and anti-inflammatory effects. Treatment with angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs) has been demonstrated to prevent atrial fibrillation and new-onset diabetes, and provide cardiac, cerebral, and renal protection. Combination therapy with ACEIs and ARBs, compared with monotherapy, provides enhanced reno- and cardioprotection, although available data indicate that combination RAS blockade may be beneficial only in select patient groups, such as those with diabetes mellitus, chronic kidney disease, or heart failure (HF). In certain high-risk patients, the use of ARBs provides comparable efficacy to that observed with ACEIs. The efficacy of these agents may stem from pleiotropic effects beyond blood pressure (BP) reduction. Several studies demonstrate achievement of clinical endpoints without significant effects on BP. Copyright © 2009 Wiley Periodicals, Inc. [source] Endogenous B-type Natriuretic Peptide: A Limb of the Regulatory Response to Acutely Decompensated Heart FailureCLINICAL CARDIOLOGY, Issue 9 2008Robert E. Hobbs MD Abstract Acutely decompensated heart failure (ADHF) represents an episodic failure of cardiorenal homeostasis that may resolve with upregulation of natriuretic peptides, bradykinin, and certain prostacyclins. B-type natriuretic peptide (BNP) has multiple favorable effects, including vasodilation, diuresis, natriuresis, and inhibition of vascular endothelial proliferation and cardiac fibrosis. By antagonizing the effects of activation of the renin-angiotensin-aldosterone system (RAAS) and the sympathetic nervous system in volume overload, the endogenous BNP response may help rescue patients from episodic ADHF. Although knowledge of BNP physiology is expanding, we still have limited understanding of the heterogeneity of proBNP-derived molecules, including active 32 amino acid BNP and less active junk BNP forms. Emerging evidence suggests that in ADHF, the endogenous BNP response is overwhelmed by neurohormonal activation. This relative BNP deficiency may also be accompanied by physiologic resistance to BNP. Additionally, abnormalities of BNP production may result in a lower proportion of active BNP relative to less active forms that may also be detected by point-of-care tests. Improved detection of the various BNP species may clarify these concepts and facilitate improved clinical management of ADHF. Copyright © 2008 Wiley Periodicals, Inc. [source] | ||||||||||||||||||||||