Research Article Renal Vascular Response to Angiotensin II Administration in Two Kidneys-One Clip Hypertensive Rats Treated with High Dose of Estradiol: The Role of Mas Receptor Samira Choopani 1,2 and Mehdi Nematbakhsh 1,2,3 1 Water and Electrolytes Research Center, Isfahan University of Medical Sciences, Isfahan, Iran 2 Department of Physiology, Isfahan University of Medical Sciences, Isfahan, Iran 3 Isfahan MN Institute of Basic and Applied Sciences Research, Isfahan, Iran Correspondence should be addressed to Mehdi Nematbakhsh; nematbakhsh@med.mui.ac.ir Received 2 November 2020; Revised 15 January 2021; Accepted 23 January 2021; Published 2 March 2021 Academic Editor: Bhagwan Satiani Copyright © 2021 Samira Choopani and Mehdi Nematbakhsh. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. 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. 1. Introduction High blood pressure caused about 9.4 million deaths and more than half of all strokes and ischemic heart diseases [1]. It is expected that more than one billion people world- wide will suffer from hypertension in 2025 [2]. 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 also exist between MasR and AT1R or AT2R [7]. The RAS component expressions are different between the sexes [4], and females are less sensitive to Ang II- induced hypertension [8] due to the higher AT2R/AT1R ratio in females [9, 10]. Response to Ang II in the female is mediated by AT2R [9] through an estrogen-dependent Hindawi International Journal of Vascular Medicine Volume 2021, Article ID 6643485, 8 pages https://doi.org/10.1155/2021/6643485