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大脑中的血管紧张素2型受体与高血压的保护作用

Protective Angiotensin Type 2 Receptors in the Brain and Hypertension.

作者信息

de Kloet Annette D, Steckelings Ulrike M, Sumners Colin

机构信息

Department of Physiology and Functional Genomics, College of Medicine, University of Florida, 1600 SW Archer Road, Box 100274, Gainesville, FL, 32610-0274, USA.

IMM - Department of Cardiovascular and Renal Research, University of Southern Denmark, Odense, Denmark.

出版信息

Curr Hypertens Rep. 2017 Jun;19(6):46. doi: 10.1007/s11906-017-0746-x.

Abstract

PURPOSE OF REVIEW

The goal of this review is to assess the evidence that activation of angiotensin type 2 receptors (AT2R) in the brain can lower blood pressure and possibly constitute an endogenous anti-hypertensive mechanism.

RECENT FINDINGS

Recent studies that detail the location of AT2R in the brain, particularly within or near cardiovascular control centers, mesh well with findings from pharmacological and gene transfer studies which demonstrate that activation of central AT2R can influence cardiovascular regulation. Collectively, these studies indicate that selective activation of brain AT2R causes moderate decreases in blood pressure in normal animals and more profound anti-hypertensive effects, along with restoration of baroreflex function, in rodent models of neurogenic hypertension. These findings have opened the door to studies that can (i) assess the role of specific AT2R neuron populations in depressing blood pressure, (ii) determine the relevance of such mechanisms, and (iii) investigate interactions between AT2R and depressor angiotensin-(1-7)/Mas mechanisms in the brain.

摘要

综述目的

本综述的目的是评估大脑中血管紧张素2型受体(AT2R)激活可降低血压并可能构成内源性抗高血压机制的证据。

最新发现

近期详细阐述大脑中AT2R位置的研究,特别是在心血管控制中心内或其附近,与药理学和基因转移研究结果相契合,这些研究表明中枢AT2R的激活可影响心血管调节。总体而言,这些研究表明,大脑AT2R的选择性激活在正常动物中可导致血压适度下降,而在神经源性高血压的啮齿动物模型中具有更显著的抗高血压作用,并伴有压力反射功能的恢复。这些发现为以下研究打开了大门:(i)评估特定AT2R神经元群体在降低血压中的作用;(ii)确定此类机制的相关性;(iii)研究大脑中AT2R与降压性血管紧张素-(1-7)/Mas机制之间的相互作用。

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