Endogenous angiotensin II in the NTS contributes to sympathetic activation in rats with aortocaval shunt.

Endogenous angiotensin II in the NTS contributes to sympathetic activation in rats with aortocaval shunt.
复制标题

NTS 中的内源性血管紧张素 II 有助于主动脉腔分流大鼠的交感神经激活。

DOI:
--
复制
发表时间:
2001
期刊:
American Journal of Physiology. Regulatory Integrative and Comparative Physiology
影响因子:
--
通讯作者:
Akira Takeshita
Akira Takeshita
中科院分区:
--
文献类型:
--
作者:
H. Shigematsu;Yoshitaka Hirooka;K. Eshima;M. Shihara;Tatsuya Tagawa;Akira Takeshita

文献摘要

参考文献

被引文献

相似文献

最近的研究表明,中枢神经系统负责激活交感神经活动(SNA)和肾素-血管紧张素系统在心力衰竭(HF)。本研究的目的是确定孤束核(NTS)内的肾素-血管紧张素系统的激活是否在HF时SNA增强中起作用。高输出HF诱导的下腔静脉(A-V)分流与一些修改的大鼠。这些大鼠表现出左心室扩张和高输出量HF的血流动力学体征。房室分流组大鼠尿儿茶酚胺排泄量和最大肾SNA(RSNA)均高于对照组。将血管紧张素II 1型受体拮抗剂CV11974微量注射到NTS中。CV11974降低房室分流大鼠的动脉压和RSNA的程度大于对照组。血管紧张素转换酶mRNA在房室分流大鼠延髓的表达明显高于对照组。这些结果表明,在NTS内的肾素-血管紧张素系统的激活有助于增强SNA在这个模型中。
Recent studies have suggested that the central nervous system is responsible for activation of sympathetic nerve activity (SNA) and the renin-angiotensin system in heart failure (HF). The aim of this study was to determine whether activation of the renin-angiotensin system within the nucleus of the solitary tract (NTS) plays a role in enhanced SNA in HF. High-output HF was induced by an aortocaval (A-V) shunt with some modifications in the rat. These rats exhibited a left ventricular dilatation and hemodynamic signs of high-output HF. Urinary catecholamine excretion and maximal renal SNA (RSNA) were greater in the A-V shunted rats than in the control rats. Microinjection of an angiotensin II type 1-receptor antagonist, CV11974, into the NTS was performed. The arterial pressure and RSNA were reduced by CV11974 to a greater degree in the A-V shunted rats than in the control rats. The expression of angiotensin-converting enzyme mRNA in the medulla was greater in the A-V shunted rats than in the control rats. These results suggest that activation of the renin-angiotensin system within the NTS contributes to an enhanced SNA in this model.
大鼠中枢神经系统中血管紧张素 II 免疫反应细胞和纤维的组织。
DOI: 10.1159/000124046
发表时间: 1985
期刊: Neuroendocrinology
影响因子: 4.1
作者:
Lind,RW;Swanson,LW;Ganten,D
通讯作者: Ganten,D
DOI: 10.1152/jappl.1994.77.6.2907
发表时间: 1994
期刊: Journal of applied physiology (Bethesda, Md. : 1985)
影响因子: --
作者:
Huang,M;LeBlanc,MH;Hester,RL
通讯作者: Hester,RL
阻断 AT1 受体可增强心力衰竭清醒兔子心率的压力反射控制。
DOI: 10.1152/ajpregu.1996.271.1.r303
发表时间: 1996
期刊: The American journal of physiology
影响因子: --
作者:
Murakami,H;Liu,JL;Zucker,IH
通讯作者: Zucker,IH
DOI: 10.1152/ajpregu.1998.275.5.r1611
发表时间: 1998-11-01
影响因子: 2.8
作者:
Matsumura, K;Averill, DB;Ferrario, CM
通讯作者: Ferrario, CM
心力衰竭的治疗:神经体液激活的作用。
DOI: 10.2169/internalmedicine.37.112
发表时间: 1998
期刊: Internal medicine (Tokyo, Japan)
影响因子: --
作者:
Middlekauff,HR;Mark,AL
通讯作者: Mark,AL