Angiotensin II enhances baroreflex control of sympathetic outflow in heart failure

Hiroshi Murakami, Jun Li Liu, Irving H Zucker

Research output: Contribution to journalArticle

62 Scopus citations

Abstract

Enhanced sympathetic outflow is seen in both patients with congestive heart failure and animals with experimental heart failure. In a previous study, we demonstrated that the baroreflex control of heart rate was impaired in conscious rabbits with pacing-induced heart failure and that this impairment wits partially restored by blockade of angiotensin II type I (AT1) receptors. In the present study, we determined the interaction between the renin-angiotensin system and baroreflex control of renal sympathetic nerve activity in normal conscious rabbits and conscious rabbits with pacing induced heart failure before and after AT1 receptor blockade. Heart failure was induced by rapid ventricular pacing at a rate of 360 to 380 beats per minute for an average of 16.7±0.6 days. To generate baroreflex curves, we altered arterial pressure by administering phenylephrine and sodium nitroprusside. A sigmoidal logistic function was fit to renal sympathetic nerve activity incan arterial pressure relationships for analysis of several components of baroreflex function. AT1 receptors were blocked by intravenous administration of the specific antagonist L-158,809. In normal rabbits, there was no significant difference in any parameter of baroreflex function before and alter blockade of ATL receptors. In contrast, blockade of AT1 receptors enhanced baroreflex sensitivity in heart failure rabbits. The maximal gain increased to 5.0±0.7% renal sympathetic nerve activity/mm Hg from 2.6±0.3 (P<.05). Although L-158,809 had no effect on baseline renal sympathetic nerve activity in normal rabbits, analysis of the data in the heart failure rabbits indicated that baseline renal sympathetic nerve activity was reduced from 33±5% to 17±4% after L-158,809 administration after adjustment for changes in arterial pressure. These data suggest that angiotensin II plays a role in barorellex impairment in this model of heart failure and may be in part responsible for the depressed baroreflex sensitivity observed in heart failure.

Original languageEnglish (US)
Pages (from-to)564-569
Number of pages6
JournalHypertension
Volume29
Issue number2
DOIs
StatePublished - Feb 1997

    Fingerprint

Keywords

  • arterial pressure
  • heart failure
  • receptors, angiotensin
  • sympathetic nervous system

ASJC Scopus subject areas

  • Internal Medicine

Cite this