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首页> 外文期刊>American Journal of Physiology >Endogenous angiotensin II in the NTS contributes to sympathetic activation in rats with aortocaval shunt.
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Endogenous angiotensin II in the NTS contributes to sympathetic activation in rats with aortocaval shunt.

机译：NTS中的内源性血管紧张素II有助于主动脉分流大鼠的交感神经激活。

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摘要

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.
机译：最近的研究表明，在心力衰竭（HF）中，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。这项研究的目的是确定孤立道（NTS）核内的肾素-血管紧张素系统的激活是否在HF中增强SNA中起作用。高输出HF是由大鼠的主动脉（A-V）分流器进行了一些修改而诱发的。这些大鼠表现出左心室扩张和高输出HF的血流动力学迹象。 A-V分流大鼠的尿儿茶酚胺排泄量和最大肾SNA（RSNA）高于对照组。将血管紧张素II型1受体拮抗剂CV11974微注射到NTS中。与对照大鼠相比，CV11974在A-V分流大鼠中的动脉压和RSNA降低程度更大。 A-V分流大鼠的髓质中血管紧张素转化酶mRNA的表达高于对照组。这些结果表明，在该模型中，NTS中肾素-血管紧张素系统的激活有助于增强SNA。

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