Role of Mas receptor antagonist (A779) in renal hemodynamics in condition of blocked angiotensin II receptors in rats.

The vasodilatory effect of angiotensin 1-7 (Ang 1-7) is exerted in the vascular bed via Mas receptor (MasR) gender dependently. However, the crosstalk between MasR and angiotensin II (Ang II) types 1 and 2 receptors (AT1R and AT2R) may change some actions of Ang 1-7 in renal circulation. In this study by blocking AT1R and AT2R, the role of MasR in kidney hemodynamics was described. In anaesthetized male and female Wistar rats, the effects of saline as vehicle and MasR blockade (A779) were tested on mean arterial pressure (MAP), renal perfusion pressure (RPP), renal blood flow (RBF), and renal vascular resistance (RVR) when both AT1R and AT2R were blocked by losartan and PD123319, respectively. In male rats, when AT1R and AT2R were blocked, there was a tendency for the increase in RBF/wet kidney tissue weight (RBF/KW) to be elevated by A779 as compared with the vehicle (P=0.08), and this was not the case in female rats. The impact of MasR on renal hemodynamics appears not to be sexual dimorphism either when Ang II receptors were blocked. It seems that co-blockade of all AT1R, AT2R, and MasR may alter RBF/ KW in male more than in female rats. These findings support a crosstalk between MasR and Ang II receptors in renal circulation.

Role of Mas receptor antagonist (A779) on pressure diuresis and natriuresis and renal blood flow in the absence of angiotensin II receptors type 1 and 2 in female and male rats.

Sexual differences in blood pressure are associated with angiotensin 1-7 (Ang1-7) and its receptor and enzyme function targeting. Blockade of angiotensin II (AngII) receptors type 1 and 2 (AT1R and AT2R) inhibits some actions of Ang1-7. We described the role of Ang1-7 receptor (MasR) antagonist (A779) on kidney hemodynamics when AT1R and AT2R are blocked with losartan and PD123319. In anaesthetized male and female rats after blockade of both AT1R and AT2R, the renal perfusion pressure (RPP) was controlled in two levels of 80 and 100 mmHg via an adjustable clamp placed around the aorta above the level of the renal arteries. Then, the effects of saline vehicle and MasR blocker (A779) were tested on pressure natriuresis and diuresis, renal blood flow (RBF), and renal vascular resistance (RVR). In the absence of AT1R and AT2R; RVR, RBF/wet kidney tissue weight, and serum level of renin did not alter in both genders either MasR was blocked or not. However, urine flow rate (UF) and sodium excretion (UNaV) increased significantly at the pressure level of 100 mmHg in the presence of MasR in male (P<0.05) but not in female rats. When AT1R and AT2R were blocked, the impact of MasR is gender-related in pressure natriuresis and diuresis, and pressure natriuresis and diuresis in male rats (not female) increases in the presence of MasR.

Apple cider vinegar attenuates lipid profile in normal and diabetic rats.

In this study, the effect of apple cider vinegar on Fasting Blood Glucose (FBG), glycated haemoglobin (HbA1c) and lipid profile in normal and diabetic rats was investigated. Diabetes was induced in male Wistar rats (300+/-30 g) by the intraperitoneal injection of streptozotocin (60 mg kg(-1) of body weight). Both normal and diabetic animals were fed with standard animal food containing apple cider vinegar (6% w/w) for 4 weeks. Fasting blood glucose did not change, while HbA1c significantly decreased by apple cider vinegar in diabetic group (p<0.05). In normal rats fed with vinegar, significant reduction of low density lipoprotein-cholesterol (LDL-c) (p<0.005) and significant increase of high density lipoprotein-cholesterol (HDL-c) levels (p<0.005) were observed. Apple cider vinegar also reduced serum triglyceride (TG) levels (p<0.005) and increased HDL-c (p<0.005) in diabetic animals. These results indicate that apple cider vinegar improved the serum lipid profile in normal and diabetic rats by decreasing serum TG, LDL-c and increasing serum HDL-c and may be of great value in managing the diabetic complications.