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pubmed-article:11353669pubmed:abstractTextRecent 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.lld:pubmed
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pubmed-article:11353669pubmed:paginationR1665-73lld:pubmed
pubmed-article:11353669pubmed:dateRevised2007-11-15lld:pubmed
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pubmed-article:11353669pubmed:articleTitleEndogenous angiotensin II in the NTS contributes to sympathetic activation in rats with aortocaval shunt.lld:pubmed
pubmed-article:11353669pubmed:affiliationDepartment of Cardiovascular Medicine, Cardiovascular Science, Graduate School of Medical Sciences, Kyushu University, Fukuoka 812-8582, Japan.lld:pubmed
pubmed-article:11353669pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:11353669pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
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