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Purpose. To assess whether renin-angiotensin system inhibitor (RASI) utilization is associated with age-related macular degeneration (AMD) prevalence among hypertensive patients. Methods. A US population-based, cross-sectional study was conducted. 3,023 hypertensive participants aged 40 years and older with gradable retinal images and ascertained RASI usage in the National Health and Nutrition Examination Survey (NHANES), 2005–2008, were finally enrolled into the study. RASI usage was obtained by interview, and AMD was determined through retinal image assessment. We performed multivariable analyses to assess the relationship between utilization of RASIs and AMD prevalence. We also took drug treatment duration into account, in order to better understand the effects of RASIs. Results. Multivariable logistic regression analyses revealed that AMD prevalence had no significant association with RASI usage but was inversely correlated with RASI treatment duration (odds ratio (OR) = 0.87, 95% confidence interval (CI) = 0.78–0.98, p = 0.02). Long-term usage (>5 years) of RASIs was significantly associated with not only reduced overall risk of AMD (OR = 0.23, 95% CI = 0.14–0.38, p < 0.001) but also lower propensity to have early (OR = 0.23, 95% CI = 0.14–0.37, p < 0.001) and late (OR = 0.25, 95% CI = 0.07–0.87, p = 0.03) AMD. Furthermore, long-term RASI users were less prone to develop soft drusen (OR = 0.67, 95% CI = 0.45–0.99, p = 0.04) and geographic atrophy (GA) (OR = 0.39, 95% CI = 0.22–0.71, p = 0.003). Conclusions. Evidence supporting that RASI utilization could directly protect against AMD in hypertensive patients was still insufficient, but long-term RASI treatment seemed to be beneficial for both early and late AMD, implicating a promising therapeutic approach that RASIs might offer for AMD prevention and management. [ABSTRACT FROM AUTHOR]

Background: Overactivation of renin-aldosterone-angiotensin system (RAS) is part of the pathogenesis of obesity-associated hypertension. Evidences have shown that weight loss can result in reduction in blood pressure and RAS. This study was aim to investigate changes of plasma aldosterone concentration (PAC) after bariatric surgery. Methods: A prospective study was done in 14 morbidly obese patients undergoing bariatric surgery. Patients who were taking medications that can interfere with PAC and renin levels were excluded. Collection of blood samples were done at baseline and at 3 and 6-month post-bariatric surgery. Results: Four out of 14 patients had hypertension at baseline. Mean body mass index (BMI) was 56.7 ± 13.5 kg/m2. PAC were significantly decreased at 3-and 6-month post-bariatric surgery from 14.3 ± 8.0 to 7.5 ± 5.5 [reduction of 36% from baseline (P < 0.01)] and 8.0 ± 6.6 ng/dl [reduction of 32% from baseline (P < 0.05)] respectively. The reduction of PAC at 3-month post-surgery was correlated with the reduction of body weight (r = 0.46, P < 0.05), waist circumference (r = 0.73, P < 0.05) and percent of body fat (r = 0.58, P < 0.05). Conclusions: Maximal reduction of PAC in obese patients underwent bariatric surgery occurred during the first 3 months after bariatric surgery. The reduction of PAC was associated with the reduction of body weight, waist circumference and percent of body fat suggesting the link between RAS and obesity-mediated hypertension. [ABSTRACT FROM AUTHOR]

The average salt intake of people in Canada, the United States, and Europe is about 3,400mg of sodium per day, which exceeds the recommended intake levels set by various health organizations. The World Health Organization recommends a worldwide reduction of sodium intake to less than 2,000mg per day. Most research to date has focused on the negative effects of high-sodium intake; however, little information is available on the metabolic effects of low-sodium intakes. This review focuses on the hormonal changes associated with low-sodium diets, specially the hormones involved in metabolism and cardiovascular and renal function. Based largely on rodent studies, low-sodium diets have been associated with changes in glycemic control, energy metabolism, cardiovascular disease risk, cholesterol concentrations, inflammation, and functioning of the renin-angiotensin-aldosterone system. Overall, research has revealed mixed results regarding the impact of dietary sodium intake on various hormones. Further research is required to assess the effects of sodium reduction on hormones and their associated pathways in order to determine the likelihood of any unintended effects. [ABSTRACT FROM AUTHOR]

Abstract: The first oral direct renin inhibitor, aliskiren, recently received approval for the treatment of hypertension. This article addresses the premise, promise, and potential limitations of this new class of renin-angiotensin system inhibitor. Although aliskiren adds to a list of more than 100 drugs approved for the treatment of hypertension, its introduction into clinical medicine is of particular interest because of the novel mechanism of action: inhibition of renin’s catalytic activity, the most proximal and rate-limiting step in renin-angiotensin system activation. By producing more complete renin-angiotensin system inhibition than with existing agents, direct renin inhibitors may afford greater protection from hypertensive complications. Other potential advantages include additional blood pressure reduction when used in combination therapy, a placebo-like side-effect profile, avid renal concentration, and long duration of action. Potential limitations include modest levels of blood pressure reduction that are equivalent to but not greater than angiotensin receptor blockers, reduced gastrointestinal absorption with a high-fat meal, and large reactive increases in renin secretion—the functional importance of which is under intense investigation. The results of outcomes trials are eagerly awaited. [Copyright &y& Elsevier]

Editorial. Comments on the therapeutic value of the renin-angiotensin system in the progression delay of chronic renal diseases in the United States. Contribution of angiotensin II type 1 (AT1) in the process of renal fibrosis; Role of hemodynamic factors in the genesis of the fibrotic response; Importance of AT1 receptor alterations in hemodynamic activity.