Blood Pressure and the Renal Actions of AT2 Receptors

被引：0
作者：
Robert M. Carey
机构：
[1] University of Virginia Health System,Division of Endocrinology and Metabolism, Department of Medicine
来源：
Current Hypertension Reports | 2017年 / 19卷
关键词：
Blood pressure; Hypertension; Angiotensin receptor; AT; receptor; Sodium excretion; Natriuresis;
D O I：
暂无
中图分类号：
学科分类号：
摘要：
Angiotensin type-2 receptors (AT2Rs) in the renal proximal tubule inhibit sodium (Na+) reabsorption by inducing renal cyclic GMP formation and internalizing and inhibiting major Na+ transporters Na+-H+ exchanger-3 (NHE-3) and Na+/K+ATPase (NKA). Instead of angiotensin II (Ang II), angiotensin III (Ang III) is the predominant endogenous agonist for this response. Exogenous non-peptide AT2R agonist Compound-21 induces natriuresis and lowers blood pressure (BP) in normal and Ang II-infused hypertensive rodents. Spontaneously hypertensive rats (SHR; both pre-hypertensive and hypertensive) have defective natriuretic responses to Ang III, suggesting a defect in AT2R-mediated natriuresis in SHR that leads to hypertension. The mechanisms of deficient AT2R-mediated natriuresis in SHR are unknown but could involve either pre-receptor or receptor/post-receptor defects.
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