Neural regulation of sympathetic nerve activity in heart failure

Irving H Zucker, Wei Wang, Marian Brändle, Harold D Schultz, Kaushik P Patel

Research output: Contribution to journalArticle

141 Citations (Scopus)

Abstract

One of the hallmarks of chronic congestive heart failure is an increase in sympathetic tone to the peripheral circulation and to the heart. A correlation between plasma norepinephrine and the severity of the heart failure state has been demonstrated. One mechanism that has been proposed to account for this sympathoexcitation is a depression in the baroreflex and, perhaps, cardiac reflex control of sympathetic nerve activity. This review summarizes work from several laboratories, including our own, that documents a depressed baroreflex control of heart rate and sympathetic nerve activity in both animals and humans with heart failure. The mechanism of the depressed baroreflex most likely is caused by reduced baroreceptor sensitivity as well as enhanced input to the central nervous system from cardiac receptors that are chemosensitive. Although sympathetic tone and arterial baroreflex sensitivity are altered in heart failure, there have been no studies showing a cause-and-effect relationship. Increases in plasma norepinephrine are similar in baroreceptor-denervated and intact dogs paced into heart failure. This latter observation calls into question the traditional concept of baroreceptor-mediated increases in sympathetic tone in heart failure.

Original languageEnglish (US)
Pages (from-to)397-414
Number of pages18
JournalProgress in Cardiovascular Diseases
Volume37
Issue number6
DOIs
StatePublished - Jan 1 1995

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Heart Failure
Baroreflex
Pressoreceptors
Norepinephrine
Reflex
Central Nervous System
Heart Rate
Observation
Dogs
Depression

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

Neural regulation of sympathetic nerve activity in heart failure. / Zucker, Irving H; Wang, Wei; Brändle, Marian; Schultz, Harold D; Patel, Kaushik P.

In: Progress in Cardiovascular Diseases, Vol. 37, No. 6, 01.01.1995, p. 397-414.

Research output: Contribution to journalArticle

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