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.

IF 2.5 Q2 PERIPHERAL VASCULAR DISEASE
International Journal of Vascular Medicine Pub Date : 2021-03-01 eCollection Date: 2021-01-01 DOI:10.1155/2021/6643485
Samira Choopani, Mehdi Nematbakhsh
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引用次数: 5

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.

Abstract Image

Abstract Image

大剂量雌二醇治疗双肾一夹高血压大鼠肾血管对血管紧张素II的反应:Mas受体的作用。
背景:高血压是世界上最重要的死亡原因之一。肾素-血管紧张素系统(RAS)和雌二醇是调节女性动脉血压的两种重要物质。然而,高血压、RAS和性激素雌二醇可能影响肾血管反应。本研究旨在确定双肾一夹(2K1C)高血压大鼠接受雌二醇治疗后,Mas受体(MasR)在血管紧张素II (Ang II)给药后肾血管反应中的作用。方法:取去卵巢大鼠进行2K1C和非2K1C治疗,同时给予雌二醇(500 μg/kg/周)或安慰剂治疗,疗程4周。随后,在麻醉下,测定分级剂量的Ang II与MasR阻断剂(A779)或其载体的肾血管反应。结果:A779或其载体对平均动脉压(MAP)、肾灌注压(RPP)和肾血流量(RBF)无明显影响。然而,在非2k1c大鼠中,Ang II输注降低了RBF,并以剂量相关的方式增加了肾血管阻力(RVR)反应(p < 0.0001)。在非2k1c大鼠中,接受A779治疗的去卵巢雌二醇治疗大鼠的反应最大(p组< 0.05)。在2K1C高血压大鼠中没有发现这些发现。例如,雌二醇处理的大鼠接受A779,在1000 ng/kg/min的Ang II输注下,非2K1C大鼠的RBF从1.6±0.2 ml/min降至0.89±0.19 ml/min, 2K1C大鼠的RBF从1.6±0.2 ml/min降至1.2±0.2 ml/min。结论:2K1C诱导的高血压可能减弱A779和雌二醇在肾血管对Angⅱ输注反应中的作用。也许,这种反应可以通过降低2K1C高血压大鼠的Ang II型1受体(AT1R)表达来解释。
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来源期刊
International Journal of Vascular Medicine
International Journal of Vascular Medicine PERIPHERAL VASCULAR DISEASE-
CiteScore
3.50
自引率
0.00%
发文量
7
审稿时长
16 weeks
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