Background. The accompanied role of Mas receptor (MasR), bradykinin (BK), and female sex hormone on renal blood flow (RBF) response to angiotensin 1-7 is not well defined. We investigated the role of MasR antagonist (A779) and BK on RBF response to Ang 1-7 infusion in ovariectomized estradiol-treated rats. Methods. Ovariectomized Wistar rats received estradiol (OVE) or vehicle (OV) for two weeks. Catheterized animals were subjected to BK and A799 infusion and mean arterial pressure (MAP), RBF, and renal vascular resistance (RVR) responses to Ang 1-7 (0, 100, and 300 ng kg−1 min−1) were determined. Results. Percentage change of RBF (%RBF) in response to Ang1-7 infusion increased in a dose-dependent manner. In the presence of BK, when MasR was not blocked, %RBF response to Ang 1-7 in OVE group was greater than OV group significantly (P < 0.05). Infusion of 300 ng kg−1 min−1 Ang 1-7 increased RBF by 6.9 ± 1.9% in OVE group versus 0.9 ± 1.8% in OV group. However when MasR was blocked, %RBF response to Ang 1-7 in OV group was greater than OVE group insignificantly. Conclusion. Coadministration of BK and A779 compared to BK alone increased RBF response to Ang 1-7 in vehicle treated rats. Such observation was not seen in estradiol treated rats.
BackgroundSeveral studies were pointed to oxidized LDL (ox-LDL) as one of the main immunogenes which have important roles in primary lesions of atherosclerosis. In this study, by immunization against ox-LDL with two different antigens in an animal model (rabbit) and consideration of its effect on two different dietary regimens; we tried to clear relation between immune system and atherosclerosis.MethodsLDL was isolated from hypercholesterolemic rabbits plasma and oxidized with MDA or Cu++. Rabbits were divided to three groups and immunized with MDA-LDL or Cu-LDL or phosphate-buffer (PBS) as a control group. Immunization was repeated after 2, 4, 6, and 8 weeks and concentration of antibodies against ox-LDL was measured in each stage. After immunization, rabbits in each group were divided to two subgroups based on the dietary regimen (fed normal or high cholesterol diet). At the beginning and the end of the study, biochemical factors were measured. Also, fatty streaks in aorta and left and right coronary arteries evaluated.ResultsImmunization with Cu2+-LDL and MDA-LDL induced statistically significant antibodies against ox-LDL. In hypercholesterolemic rabbits immunized with MDA-LDL the level of cholesterol, LDL-cholesterol, triglyceride, fasting blood sugar and fatty streak lesions in aorta and right coronary arteries were significantly decreased as compared with non-immunized high-cholesterol group. Immunization with Cu2+-LDL in hypercholesterolemic rabbits significantly decreased triglyceride, fasting blood sugar, cholesterol and CRP. No significant differences were detected in the fatty streak lesions in this group as compared with non-immunized high-cholesterol diet. In groups under normal diet immunized with MDA-LDL or Cu2+-LDL no significant effect on biochemical factors and atherosclerotic lesions were observed.ConclusionThis study indicates that although the effect of produced antibodies in several methods and different dietary regimens is different, immunization against ox-LDL is antiatherogenic.
Background: Obesity is common worldwide, especially in low- and middle-income countries. Aims: To update data on the prevalence of overweight, obesity and central obesity, and to measure incidence rates for such outcomes in adults living in the south-east of the Islamic Republic of Iran. Methods: We enrolled 9997 adults (aged 15–80 years) between 2014 and 2018 (phase 2); 2820 of whom had participated in phase 1 (2009–2011). Participants were examined for overweight, obesity, central obesity, diabetes, hypertension, low physical activity, and dyslipidaemia. Univariate and multivariate logistic regression models were used to determine the potential predictors of overweight, obesity and central obesity, and adjusted odds ratios (AOR) were obtained. Incidence rate of overweight, obesity and central obesity was reported among those who had none of these outcomes in phase 1. Results: The prevalence was 35.8% (37% men, 35% women) for overweight, 22.3% (16% men, 26.3% women) for obesity, and 31.1% (15.6% men, 41.2% women) for central obesity. The prevalence of overweight/obesity was significantly associated with age (AOR = 2.8–7.4), higher education (AOR = 1.7), female gender (AOR = 1.4), low physical activity (AOR = 1.3), smoking (AOR = 0.55) and opium use (AOR = 0.79). The prevalence increased from 33.3% to 35.8% for overweight and from 15.4% to 22.3% for obesity between phases 1 and 2. The incidence rate per 100 person-years was 5.5 for overweight, 4.7 for obesity and 2.9 for central obesity. Conclusion: Prevalence of overweight and obesity increased over 5 years. Middle-aged participants, women, and those with low physical activity were at higher risk for overweight/obesity.
Abstract- Renin angiotensin (RAS), kallikrein kinin (KKS), and sex hormonal systems demonstrate a complex contribution in kidney circulation. This study was designed to investigate the role of angiotensin 1-7 (Ang 1-7) receptor (MasR) and of bradykinin B2 receptor (B2R) in renal blood flow (RBF) response to Ang 1-7 infusion in ovariectomized estradiol treated rats. The ovariectomized rats received intramuscular vehicle (group 1, OV) or estradiol valerate (500 µg/Kg/week) (group 2, OVE) for two weeks. Then each group was divided into two subgroups subjected to receive B2R antagonist (HOE-140, subgroup A), or MasR antagonist (A779) plus HOE-140 (subgroup B). RBF and renal vascular resistance (RVR) responses to graded Ang 1-7 infusion were determined. In condition of B2R alone blocking, RBF response to Ang 1-7 in OVE group was significantly greater than that of OV group (P=0.05), however this response difference was failed by co-blockades of MasR and B2R. Estradiol could promote RBF response to graded Ang 1-7 infusion in the absence of B2R alone, however when both receptors (MasR and B2R) were blocked the role of estradiol was limited.
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