Angiotensin II and sympathoactivation in heart failure

Steven R. Goldsmith

Research output: Contribution to journalArticlepeer-review

16 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)139-145
Number of pages7
JournalJournal of cardiac failure
Issue number2
StatePublished - Jun 1999
Externally publishedYes

Bibliographical note

Funding Information:
Supported in part by a grant-in-aid from the American Heart Association, Dallas, TX; and grant no. HL-32427 fiom the National Institutes of Health, Bethesda, MD. Manuscript received December 17, 1998; revised manuscript received March 3, 1999; revised manuscript accepted March 3, 1999. Reprint requests: Steven R. Goldsmith, MD, Hennepin County Medical Center, Cardiology Division, 701 Park Avenue, Minneapolis, MN 55415. Copyright © 1999 by Churchill Livingstone ® 1071-9164/99/0502-0009510.00/0 even of increases in markers for systemic sympathoacti-vation (3). Sympathoactivation becomes more significant as the syndrome progresses, but because it occurs in patients with normal blood pressure and normal resting cardiac output, it is unlikely that such mechanisms as baroreflex deactivation contribute in the chronic state. During acute decompensation, there may be a further increase in sympathetic activity attributable to hemodynamic abnormality and baroreflex deactivation, but because baroreflexes are short-term controllers and adapt over time to changes in loading conditions (4), it is unlikely that chronic baroreceptor deactivation causes sustained sympathoactivation.


  • Angiotensin II
  • Baroreflexes
  • Catecholamines
  • Heart failure
  • Hypertension
  • Sympathetic nervous system


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