The interaction of angiotensin II and osmolality in the generation of sympathetic tone during changes in dietary salt intake

An hypothesis

Virginia Brooks, Karie E. Scrogin, Donogh F. McKeogh

Research output: Contribution to journalArticle

36 Citations (Scopus)

Abstract

At rest, sympathetic nerves exhibit tonic activity which contributes to arterial pressure maintenance. Significant evidence suggests that the absolute level of sympathetic tone is altered in a number of physiologic and pathophysiologic states. However, the mechanisms by which such changes in sympathetic tone occur are incompletely understood. The purpose of this review is to present evidence that humoral factors are essential in these changes and to detail specifically an hypothesis for the mechanisms that underlie the changes in sympathetic tone that are produced during increases or decreases in dietary salt intake. It is proposed that the net effect of changes in dietary salt on sympathetic activity is determined by the balance between simultaneous and parallel sympathoinhibitory and sympathoexcitatory humoral mechanisms. A key element of the sympathoinhibitory mechanism is the chronic sympathoexcitatory effects of angiotensin II (ANG II). When salt intake increases, ANG II levels fall, and the sympathoexcitatory actions of ANG II are lost. Simultaneously, a sympathoexcitatory pathway is triggered, possibly via increases in osmolality which activate osmoreceptors or sodium receptors. In normal individuals, the sympathoinhibitory effects of increased salt predominate, sympathetic activity decreases, and arterial pressure remains normal despite salt and water retention. However, in subjects with salt-sensitive hypertension, it appears that the sympathoexcitatory effects of salt predominate, possibly due to an inability to adequately suppress the levels or actions of ANG II. The net result, therefore, is an inappropriate increase in sympathetic activity during increased dietary salt which may contribute to the hypertensive process.

Original languageEnglish (US)
Pages (from-to)380-394
Number of pages15
JournalAnnals of the New York Academy of Sciences
Volume940
StatePublished - 2001

Fingerprint

Angiotensin II
Osmolar Concentration
Salts
Arterial Pressure
Intake
Interaction
Salt
Sodium
Maintenance
Hypertension
Water

Keywords

  • Angiotensin II
  • Baroreceptor reflex
  • Salt-sensitive hypertension
  • Sodium chloride
  • Sympathetic nervous system

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)

Cite this

@article{894ce89f5ed5491594e3233d3c037cdd,
title = "The interaction of angiotensin II and osmolality in the generation of sympathetic tone during changes in dietary salt intake: An hypothesis",
abstract = "At rest, sympathetic nerves exhibit tonic activity which contributes to arterial pressure maintenance. Significant evidence suggests that the absolute level of sympathetic tone is altered in a number of physiologic and pathophysiologic states. However, the mechanisms by which such changes in sympathetic tone occur are incompletely understood. The purpose of this review is to present evidence that humoral factors are essential in these changes and to detail specifically an hypothesis for the mechanisms that underlie the changes in sympathetic tone that are produced during increases or decreases in dietary salt intake. It is proposed that the net effect of changes in dietary salt on sympathetic activity is determined by the balance between simultaneous and parallel sympathoinhibitory and sympathoexcitatory humoral mechanisms. A key element of the sympathoinhibitory mechanism is the chronic sympathoexcitatory effects of angiotensin II (ANG II). When salt intake increases, ANG II levels fall, and the sympathoexcitatory actions of ANG II are lost. Simultaneously, a sympathoexcitatory pathway is triggered, possibly via increases in osmolality which activate osmoreceptors or sodium receptors. In normal individuals, the sympathoinhibitory effects of increased salt predominate, sympathetic activity decreases, and arterial pressure remains normal despite salt and water retention. However, in subjects with salt-sensitive hypertension, it appears that the sympathoexcitatory effects of salt predominate, possibly due to an inability to adequately suppress the levels or actions of ANG II. The net result, therefore, is an inappropriate increase in sympathetic activity during increased dietary salt which may contribute to the hypertensive process.",
keywords = "Angiotensin II, Baroreceptor reflex, Salt-sensitive hypertension, Sodium chloride, Sympathetic nervous system",
author = "Virginia Brooks and Scrogin, {Karie E.} and McKeogh, {Donogh F.}",
year = "2001",
language = "English (US)",
volume = "940",
pages = "380--394",
journal = "Annals of the New York Academy of Sciences",
issn = "0077-8923",
publisher = "Wiley-Blackwell",

}

TY - JOUR

T1 - The interaction of angiotensin II and osmolality in the generation of sympathetic tone during changes in dietary salt intake

T2 - An hypothesis

AU - Brooks, Virginia

AU - Scrogin, Karie E.

AU - McKeogh, Donogh F.

PY - 2001

Y1 - 2001

N2 - At rest, sympathetic nerves exhibit tonic activity which contributes to arterial pressure maintenance. Significant evidence suggests that the absolute level of sympathetic tone is altered in a number of physiologic and pathophysiologic states. However, the mechanisms by which such changes in sympathetic tone occur are incompletely understood. The purpose of this review is to present evidence that humoral factors are essential in these changes and to detail specifically an hypothesis for the mechanisms that underlie the changes in sympathetic tone that are produced during increases or decreases in dietary salt intake. It is proposed that the net effect of changes in dietary salt on sympathetic activity is determined by the balance between simultaneous and parallel sympathoinhibitory and sympathoexcitatory humoral mechanisms. A key element of the sympathoinhibitory mechanism is the chronic sympathoexcitatory effects of angiotensin II (ANG II). When salt intake increases, ANG II levels fall, and the sympathoexcitatory actions of ANG II are lost. Simultaneously, a sympathoexcitatory pathway is triggered, possibly via increases in osmolality which activate osmoreceptors or sodium receptors. In normal individuals, the sympathoinhibitory effects of increased salt predominate, sympathetic activity decreases, and arterial pressure remains normal despite salt and water retention. However, in subjects with salt-sensitive hypertension, it appears that the sympathoexcitatory effects of salt predominate, possibly due to an inability to adequately suppress the levels or actions of ANG II. The net result, therefore, is an inappropriate increase in sympathetic activity during increased dietary salt which may contribute to the hypertensive process.

AB - At rest, sympathetic nerves exhibit tonic activity which contributes to arterial pressure maintenance. Significant evidence suggests that the absolute level of sympathetic tone is altered in a number of physiologic and pathophysiologic states. However, the mechanisms by which such changes in sympathetic tone occur are incompletely understood. The purpose of this review is to present evidence that humoral factors are essential in these changes and to detail specifically an hypothesis for the mechanisms that underlie the changes in sympathetic tone that are produced during increases or decreases in dietary salt intake. It is proposed that the net effect of changes in dietary salt on sympathetic activity is determined by the balance between simultaneous and parallel sympathoinhibitory and sympathoexcitatory humoral mechanisms. A key element of the sympathoinhibitory mechanism is the chronic sympathoexcitatory effects of angiotensin II (ANG II). When salt intake increases, ANG II levels fall, and the sympathoexcitatory actions of ANG II are lost. Simultaneously, a sympathoexcitatory pathway is triggered, possibly via increases in osmolality which activate osmoreceptors or sodium receptors. In normal individuals, the sympathoinhibitory effects of increased salt predominate, sympathetic activity decreases, and arterial pressure remains normal despite salt and water retention. However, in subjects with salt-sensitive hypertension, it appears that the sympathoexcitatory effects of salt predominate, possibly due to an inability to adequately suppress the levels or actions of ANG II. The net result, therefore, is an inappropriate increase in sympathetic activity during increased dietary salt which may contribute to the hypertensive process.

KW - Angiotensin II

KW - Baroreceptor reflex

KW - Salt-sensitive hypertension

KW - Sodium chloride

KW - Sympathetic nervous system

UR - http://www.scopus.com/inward/record.url?scp=0034937212&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0034937212&partnerID=8YFLogxK

M3 - Article

VL - 940

SP - 380

EP - 394

JO - Annals of the New York Academy of Sciences

JF - Annals of the New York Academy of Sciences

SN - 0077-8923

ER -