The regulation of sympathetic outflow in heart failure

The roles of angiotensin II, nitric oxide, and exercise training

Irving H Zucker, Wei Wang, Rainer U. Pliquett, Jun Li Liu, Kaushik P Patel

Research output: Contribution to journalArticle

74 Citations (Scopus)

Abstract

Sympatho-excitation is a hallmark of the chronic heart failure (CHF) state. It has long been assumed that this sympatho-excitation is mediated by a reduction in sensory input from cardiopulmonary and arterial baroreceptors. However, recent data suggest that these reflexes may only be important in the initiation of the sympatho-excitatory state and may not be necessary for the sustained increase in sympathetic nerve activity (SNA) in CHF. Two humoral factors that can influence SNA are nitric oxide (NO) and angiotensin II (AngII). Animals with CHF exhibit a downregulation in central gene expression for the neuronal isoform of nitric oxide synthase (nNOS). In addition, blockade of AngII receptors in combination with NO donation reduces SNA in animals with CHF, while NO donation alone has no effect on SNA. Chronic exercise training (EX) reduces both plasma AngII and SNA in rabbits with CHF while improving baroreflex function. Blockade of AT 1 receptors enhances baroreflex function in non-EX CHF rabbits, but has little effect in EX CHF rabbits. These data suggest that the sympatho-excitatory state that is typical of CHF is, in part, due to changes in AngII and NO. Depressed baroreflex function and the elevated SNA can be improved by EX in animals with CHF.

Original languageEnglish (US)
Pages (from-to)431-443
Number of pages13
JournalAnnals of the New York Academy of Sciences
Volume940
StatePublished - Jan 1 2001

Fingerprint

Angiotensin II
Nitric Oxide
Heart Failure
Exercise
Baroreflex
Animals
Rabbits
Nitric Oxide Synthase Type I
Pressoreceptors
Angiotensin Receptors
Gene expression
Nitric Oxide Synthase
Reflex
Nerve
Protein Isoforms
Down-Regulation
Plasmas
Gene Expression
Rabbit

Keywords

  • Angiotensin II
  • Chronic heart failure
  • Exercise training
  • Nitric oxide
  • Sympathetic nerve activity
  • Sympatho-excitation

ASJC Scopus subject areas

  • Neuroscience(all)
  • Biochemistry, Genetics and Molecular Biology(all)
  • History and Philosophy of Science

Cite this

The regulation of sympathetic outflow in heart failure : The roles of angiotensin II, nitric oxide, and exercise training. / Zucker, Irving H; Wang, Wei; Pliquett, Rainer U.; Liu, Jun Li; Patel, Kaushik P.

In: Annals of the New York Academy of Sciences, Vol. 940, 01.01.2001, p. 431-443.

Research output: Contribution to journalArticle

@article{702d692ca70b4be7997e4d3135a4c922,
title = "The regulation of sympathetic outflow in heart failure: The roles of angiotensin II, nitric oxide, and exercise training",
abstract = "Sympatho-excitation is a hallmark of the chronic heart failure (CHF) state. It has long been assumed that this sympatho-excitation is mediated by a reduction in sensory input from cardiopulmonary and arterial baroreceptors. However, recent data suggest that these reflexes may only be important in the initiation of the sympatho-excitatory state and may not be necessary for the sustained increase in sympathetic nerve activity (SNA) in CHF. Two humoral factors that can influence SNA are nitric oxide (NO) and angiotensin II (AngII). Animals with CHF exhibit a downregulation in central gene expression for the neuronal isoform of nitric oxide synthase (nNOS). In addition, blockade of AngII receptors in combination with NO donation reduces SNA in animals with CHF, while NO donation alone has no effect on SNA. Chronic exercise training (EX) reduces both plasma AngII and SNA in rabbits with CHF while improving baroreflex function. Blockade of AT 1 receptors enhances baroreflex function in non-EX CHF rabbits, but has little effect in EX CHF rabbits. These data suggest that the sympatho-excitatory state that is typical of CHF is, in part, due to changes in AngII and NO. Depressed baroreflex function and the elevated SNA can be improved by EX in animals with CHF.",
keywords = "Angiotensin II, Chronic heart failure, Exercise training, Nitric oxide, Sympathetic nerve activity, Sympatho-excitation",
author = "Zucker, {Irving H} and Wei Wang and Pliquett, {Rainer U.} and Liu, {Jun Li} and Patel, {Kaushik P}",
year = "2001",
month = "1",
day = "1",
language = "English (US)",
volume = "940",
pages = "431--443",
journal = "Annals of the New York Academy of Sciences",
issn = "0077-8923",
publisher = "Wiley-Blackwell",

}

TY - JOUR

T1 - The regulation of sympathetic outflow in heart failure

T2 - The roles of angiotensin II, nitric oxide, and exercise training

AU - Zucker, Irving H

AU - Wang, Wei

AU - Pliquett, Rainer U.

AU - Liu, Jun Li

AU - Patel, Kaushik P

PY - 2001/1/1

Y1 - 2001/1/1

N2 - Sympatho-excitation is a hallmark of the chronic heart failure (CHF) state. It has long been assumed that this sympatho-excitation is mediated by a reduction in sensory input from cardiopulmonary and arterial baroreceptors. However, recent data suggest that these reflexes may only be important in the initiation of the sympatho-excitatory state and may not be necessary for the sustained increase in sympathetic nerve activity (SNA) in CHF. Two humoral factors that can influence SNA are nitric oxide (NO) and angiotensin II (AngII). Animals with CHF exhibit a downregulation in central gene expression for the neuronal isoform of nitric oxide synthase (nNOS). In addition, blockade of AngII receptors in combination with NO donation reduces SNA in animals with CHF, while NO donation alone has no effect on SNA. Chronic exercise training (EX) reduces both plasma AngII and SNA in rabbits with CHF while improving baroreflex function. Blockade of AT 1 receptors enhances baroreflex function in non-EX CHF rabbits, but has little effect in EX CHF rabbits. These data suggest that the sympatho-excitatory state that is typical of CHF is, in part, due to changes in AngII and NO. Depressed baroreflex function and the elevated SNA can be improved by EX in animals with CHF.

AB - Sympatho-excitation is a hallmark of the chronic heart failure (CHF) state. It has long been assumed that this sympatho-excitation is mediated by a reduction in sensory input from cardiopulmonary and arterial baroreceptors. However, recent data suggest that these reflexes may only be important in the initiation of the sympatho-excitatory state and may not be necessary for the sustained increase in sympathetic nerve activity (SNA) in CHF. Two humoral factors that can influence SNA are nitric oxide (NO) and angiotensin II (AngII). Animals with CHF exhibit a downregulation in central gene expression for the neuronal isoform of nitric oxide synthase (nNOS). In addition, blockade of AngII receptors in combination with NO donation reduces SNA in animals with CHF, while NO donation alone has no effect on SNA. Chronic exercise training (EX) reduces both plasma AngII and SNA in rabbits with CHF while improving baroreflex function. Blockade of AT 1 receptors enhances baroreflex function in non-EX CHF rabbits, but has little effect in EX CHF rabbits. These data suggest that the sympatho-excitatory state that is typical of CHF is, in part, due to changes in AngII and NO. Depressed baroreflex function and the elevated SNA can be improved by EX in animals with CHF.

KW - Angiotensin II

KW - Chronic heart failure

KW - Exercise training

KW - Nitric oxide

KW - Sympathetic nerve activity

KW - Sympatho-excitation

UR - http://www.scopus.com/inward/record.url?scp=0034930734&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0034930734&partnerID=8YFLogxK

M3 - Article

VL - 940

SP - 431

EP - 443

JO - Annals of the New York Academy of Sciences

JF - Annals of the New York Academy of Sciences

SN - 0077-8923

ER -