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

Hideaki Shigematsu, Yoshitaka Hirooka, Kenichi Eshima, Miwako Shihara, Tatsuya Tagawa, Akira Takeshita

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    28 Citations (Scopus)

    Abstract

    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.

    Original languageEnglish
    Pages (from-to)R1665-R1673
    JournalAmerican Journal of Physiology - Regulatory Integrative and Comparative Physiology
    Volume280
    Issue number6 49-6
    DOIs
    Publication statusPublished - 2001

    All Science Journal Classification (ASJC) codes

    • Physiology
    • Physiology (medical)

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