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限水增加大鼠脑桥和下丘脑室旁核血管紧张素转换酶但不增加血管紧张素 AT(1) 受体的表达。

Water deprivation increases angiotensin-converting enzyme but not AT(1) receptor expression in brainstem and paraventricular nucleus of the hypothalamus of the rat.

机构信息

Department of Pharmacology, School of Pharmacy, University of Mississippi, University, MS 38677, USA.

出版信息

Brain Res. 2010 Mar 10;1319:83-91. doi: 10.1016/j.brainres.2009.12.079. Epub 2010 Jan 4.

DOI:10.1016/j.brainres.2009.12.079
PMID:20051229
Abstract

The rostral ventrolateral medulla (RVLM) is critical to the maintenance of blood pressure. It has been proposed that blood-borne Ang II can influence the RVLM via a neural connection between the circumventricular organs and paraventricular nucleus of the hypothalamus (PVH) and that a component of this pathway is angiotensinergic. A period of water deprivation leads to increased ability of angiotensin type 1 (AT(1)) receptor antagonists to reduce blood pressure when administered into the RVLM and PVH. We studied the differences in AT(1) receptor and angiotensin-converting enzyme (ACE) expression in these and other brain regions involved in blood pressure regulation and water intake following dehydration. AT(1) receptor and ACE expression in brains of rats deprived of water for 48 h were compared to that of water-replete rats by quantitative receptor autoradiography. AT(1) receptor expression was increased in the subfornical organ and periventricular nucleus of the hypothalamus, but not in other brain regions measured. ACE expression was increased in the RVLM, PVH, choroid plexus, median preoptic nucleus, and organosum vasculosum of the lamina terminalis. These findings suggest that increased Ang II production but not increased receptor expression in the PVH and RVLM is the mechanism by which Ang II in the brain helps to sustain systemic blood pressure during periods of water deprivation.

摘要

延髓头端腹外侧区(RVLM)对血压的维持至关重要。有人提出,血液中的血管紧张素 II 可以通过脑室内器官和下丘脑室旁核(PVH)之间的神经连接来影响 RVLM,并且该途径的一个组成部分是血管紧张素能的。一段时间的缺水会导致血管紧张素 1 型(AT1)受体拮抗剂在 RVLM 和 PVH 给药时降低血压的能力增加。我们研究了在这些和其他参与血压调节和水摄入的脑区中,AT1 受体和血管紧张素转换酶(ACE)表达在脱水后的差异。通过定量受体放射自显影术比较了缺水 48 小时的大鼠和水充足的大鼠的大脑中的 AT1 受体和 ACE 表达。在脑室内器官和下丘脑室旁核中,AT1 受体表达增加,但在测量的其他脑区中没有增加。ACE 表达在 RVLM、PVH、脉络丛、中脑视前核和终板血管器官中增加。这些发现表明,在 PVH 和 RVLM 中,Ang II 产生增加而不是受体表达增加,是脑内 Ang II 在缺水期间帮助维持全身血压的机制。

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