Angiotensin-mediated increase in renal sympathetic nerve discharge within the PVN: role of nitric oxide
Angiotensin-mediated increase in renal sympathetic nerve discharge within the PVN: role of nitric oxide
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DOI：
10.1152/ajpregu.00338.2004
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发表时间：
2006-04-01
影响因子：
2.8
通讯作者：
Patel, KP
中科院分区：
文献类型：
--
作者：
Li, YF;Wang, W;Patel, KP
血管紧张素介导的PVN内肾交感神经放电增加：一氧化氮的作用。 Am J Physiol Regul Integr Comp Physiol 290：R1035 - R1043，2006 年。首次发表于 2005 年 12 月 1 日； doi：10.1152/ajpregu。 00338.2004。 - 已知下丘脑的室旁核（PVN）是中枢神经系统交感神经流出整合的重要部位。 ANG II 和一氧化氮 (NO) 在调节交感神经活动中发挥重要作用。本研究的目的是检查PVN内NO和ANG II之间的相互作用如何影响大鼠的交感神经流出。测量肾交感神经放电（RSND）、动脉血压（AP）和心率（HR），以响应将ANG II和N-G-单甲基-v1-L-精氨酸（L-NMMA）施用到PVN中。将 ANG II（0.05、0.5 和 1.0 nmol）显微注射到 PVN 中，RSND、AP 和 HR 以剂量依赖性方式增加，导致在最高剂量下，相对于基线分别增加 53 +/- 9%、19 +/- 3 mmHg 和 32 +/- 12 次/分钟。预先显微注射 L-NMMA 显着增强了这些反应，并被 ANG II 1 型受体拮抗剂氯沙坦阻断。类似地，在 PVN 内给予神经元 NO 合酶反义也增强了 ANG II 反应。相反，腺病毒基因转移导致 PVN 内神经元 NOS 的过度表达显着减弱了 ANG II 反应。将 ANG II (1 nmol) 推拉给药至 PVN 诱导 NO 释放增加。我们的数据表明，PVN 内的 ANG II 1 型受体介导对 RSND、AP 和 HR 的兴奋作用。 PVN 中的 NO 可由 ANG II 刺激诱导，进而抑制 ANG II 介导的交感神经活动增加。 PVN 内的这种负反馈机制可能在维持交感神经流出的整体平衡和音调方面发挥重要作用。
Angiotensin-mediated increase in renal sympathetic nerve discharge within the PVN: role of nitric oxide. Am J Physiol Regul Integr Comp Physiol 290: R1035 - R1043, 2006. First published December 1, 2005; doi: 10.1152/ajpregu. 00338.2004. - The paraventricular nucleus ( PVN) of the hypothalamus is known to be an important site of integration in the central nervous system for sympathetic outflow. ANG II and nitric oxide ( NO) play an important role in regulation of sympathetic nerve activity. The purpose of the present study was to examine how the interaction between NO and ANG II within the PVN affects sympathetic outflow in rats. Renal sympathetic nerve discharge (RSND), arterial blood pressure (AP), and heart rate (HR) were measured in response to administration of ANG II and N-G-monomethy-vl-L-arginine (L-NMMA) into the PVN. Microinjection of ANG II (0.05, 0.5, and 1.0 nmol) into the PVN increased RSND, AP, and HR in a dose-dependent manner, resulting in increases of 53 +/- 9%, 19 +/- 3 mmHg, and 32 +/- 12 beats/min from baseline, respectively, at the highest dose. These responses were significantly enhanced by prior microinjection of L-NMMA and were blocked by losartan, an ANG II type 1 receptor antagonist. Similarly, administration of antisense to neuronal NO synthase within the PVN also potentiated the ANG II responses. Conversely, overexpression of neuronal NOS within the PVN with adenoviral gene transfer significantly attenuated ANG II responses. Push-pull administration of ANG II (1 nmol) into the PVN induced an increase in NO release. Our data indicate that ANG II type 1 receptors within the PVN mediate an excitatory effect on RSND, AP, and HR. NO in the PVN, which can be induced by ANG II stimulation, in turn inhibits the ANG II-mediated increase in sympathetic nerve activity. This negative-feedback mechanism within the PVN may play an important role in maintaining the overall balance and tone of sympathetic outflow.