Angiotensin II and sympathoactivation in heart failure.
Excessive activity of the sympathetic nervous system (SNS) contributes to the development and progression of the syndrome of congestive heart failure (CHF) in patients with decreased left ventricular function. The factors underlying chronic sympathoactivation are poorly understood, particularly in stable patients. This review summarizes both clinical and experimental data regarding the effects of angiotensin II (A-II) on the activity of the SNS. The focus is on both the direct effects of A-II on the SNS and an indirect effect medicated through alteration in function of the baroreflex. Available evidence is consistent with a potentially important effect of A-II on SNS activity, perhaps most likely via the baroreflex. Important issues regarding the direct effect of A-II on regional SNS activity, and on the physiological relevance of effects seen only at high plasma concentration of A-II remain to be fully elucidated.
Goldsmith
S R
SR
Hennepin County Medical Center, Cardiology Division, Minneapolis, MN 55415, USA.
D000804:Angiotensin II / Q000378:metabolism* / Q000494:pharmacology*; D000818:Animals; D002986:Clinical Trials as Topic; D004195:Disease Models, Animal; D006333:Heart Failure / Q000175:diagnosis / Q000503:physiopathology*; D006439:Hemodynamics / Q000187:drug effects / Q000502:physiology; D006801:Humans; D011379:Prognosis; D051381:Rats; D012084:Renin-Angiotensin System / Q000187:drug effects* / Q000502:physiology; D014662:Vasoconstrictor Agents / Q000494:pharmacology
D014662:Vasoconstrictor Agents; D000804:Angiotensin II