Angiotensin AT2 receptors and the baroreflex control of renal sympathetic nerve activity.
Angiotensin AT2 receptors and the baroreflex control of renal sympathetic nerve activity.
复制标题
血管紧张素 AT2 受体和压力反射控制肾交感神经活动。
DOI：
10.1111/apha.12240
复制
发表时间：
2014
期刊：
影响因子：
--
通讯作者：
Wainford,RD
中科院分区：
文献类型：
--
作者：
Wainford,RD
In this issue, there is an important article by Abdulla and Johns (Abdulla & Johns, 2014), which details a previously unknown role of brain nitric oxide (NO) in the modulation of central angiotensin II (type 2) receptor (AT2 receptor) stimulated high-pressure baroreflex control of heart rate (HR) and renal sympathetic nerve activity (RSNA). The authors provide the first experimental evidence that there is a facilitatory role for brain AT2 receptors in the high-pressure baroreflex regulation of RSNA and HR that is dependent of the presence of an operational central nitric oxide/nitric oxide synthase (NOS) system. These findings deepen our understanding of the interplay between brain NO and the angiotensin AT2 receptor system that acts to influence the cardiac and renal sympathetic baroreflex. Collectively, the presented studies highlight the complex interactions between brain angiotensin II (type 1)(AT1 receptor)(inhibitory) and angiotensin II (type 2)(stimulatory) receptors on the baroreflex response that is dependent on the actions of NO within the central nervous system (CNS). Owing to the significant adverse health impact of an impaired baroreflex response (Gerristen et al. 2001) studies such as these, which enhance our understanding of the baroreflex, have potential high significance for human health.Multiple studies have demonstrated an action of brain NO, likely as a neurotransmitter or neuromodulator, on central sympathetic outflow and systemic cardiovascular function. Importantly NOS activity within the nucleus tractus solitarius (NTS), which evokes depressed baroreflex regulation of blood pressure and increased central sympathetic outflow, is established as a contributing factor in the neural mechanisms underlying the development of hypertension (Chan & Chan, 2013). Further, a role of endogenous NO in the stimulation of RSNA via NTS angiotensin AT1-receptors located within the NTS has been reported (Eshima et al. 2000). Recent immunolabeling studies have provided evidence that in neurons of the NTS angiotensin AT2 receptors are required to facilitate enhanced NO production following AT1 receptor antagonism–suggesting a potential interaction between AT1 and AT2 receptors upon NO (Wang et al. 2012). Functional in-vitro studies have also demonstrated that NO blockade is able to inhibit the angiotensin AT2 stimulated facilitation of neuronal membrane potassium currents (Gao & Zucker, 2010), data which supports a potential interaction between NO and the AT2 receptor. A recent paper from the lab of Dr Johns provided in-vivo evidence, generated in rats, that in response to the physiological
