Abstract
Backgrounds High blood pressure is one of the most important causes of death around the world. The renin-angiotensin system (RAS) and estradiol are two important items that regulate arterial blood pressure in women. However, hypertension, RAS, and sex hormone estradiol may influence renal vascular responses. This study was designed to determine the role of Mas receptor (MasR) on renal vascular response to angiotensin II (Ang II) administration in two kidneys-one clip (2K1C) hypertensive rats treated with estradiol. Method The ovariectomized rats were subjected to 2K1C or non-2K1C and simultaneously treated with estradiol (500 μg/kg/weekly) or placebo for a period of 4 weeks. Subsequently, under anesthesia, renal vascular responses to graded doses of Ang II administration with MasR blockade (A779) or its vehicle were determined. Results A779 or its vehicle did not alter mean arterial pressure (MAP), renal perfusion pressure (RPP), and renal blood flow (RBF). However, in non-2K1C rats, Ang II infusion decreased RBF and increased renal vascular resistance (RVR) responses in a dose-related manner (Ptreat < 0.0001). The greatest responses were found in ovariectomized estradiol-treated rats that received A779 (Pgroup < 0.05) in non-2K1C rats. Such findings were not detected in 2K1C hypertensive rats. For example, in estradiol-treated rats that received A779, at 1000 ng/kg/min of Ang II infusion, RBF reduced from 1.6 ± 0.2 to 0.89 ± 0.19 ml/min in non-2K1C rats, and it reduced from 1.6 ± 0.2 to 1.2 ± 0.2 ml/min in 2K1C rats. Conclusion Hypertension induced by 2K1C may attenuate the role of A779 and estradiol in renal vascular responses to Ang II infusion. Perhaps, this response can be explained by the reduction of Ang II type 1 receptor (AT1R) expression in the 2K1C hypertensive rats.
Highlights
High blood pressure caused about 9.4 million deaths and more than half of all strokes and ischemic heart diseases [1]
No significant differences were observed in basal systolic blood pressure (SBP), mean arterial pressure (MAP), renal perfusion pressure (RPP), and renal blood flow (RBF) normalized to left kidney weight (RBF/gLKW) during the equilibrium period before administration of A779 or its vehicle (Table 1)
There was a little change in MAP and RPP (Ptreat ≤ 0:05) responses to A779 or its vehicle infusion in non-2K1C rats, no difference was detected between the subgroups of A779 and its vehicle
Summary
High blood pressure caused about 9.4 million deaths and more than half of all strokes and ischemic heart diseases [1]. Renal artery stenosis is responsible for hypertension in 2-4% of patients, and fibromuscular dysplasia and atherosclerosis obliterans are the two types of renovascular hypertension [3]. The renin-angiotensin system (RAS) [4] and estradiol [5] are two important items which regulate arterial blood pressure in women and need to be considered in hypertension condition. Angiotensin (Ang) II insert its effects by two types of 1&2 receptors (AT1R and AT2R), while Ang 1-7 acts via Mas receptor (MasR) [6]. Heterodimerization and functional interactions exist between MasR and AT1R or AT2R [7]
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