Excess dietary salt intake alters the excitability of central sympathetic networks

Sean D. Stocker, Christopher J. Madden, Alan F. Sved

Research output: Contribution to journalArticle

40 Citations (Scopus)

Abstract

The ingestion of excess dietary salt (defined as NaCl) is strongly correlated with cardiovascular disease, morbidity, mortality, and is regarded as a major contributing factor to the pathogenesis of hypertension. Although several mechanisms contribute to the adverse consequences of dietary salt intake, accumulating evidence suggests that dietary salt loading produces neurogenically-mediated increases in total peripheral resistance to raise arterial blood pressure (ABP). Evidence from clinical studies and experimental models clearly establishes a hypertensive effect of dietary salt loading in a subset of individuals who are deemed "salt-sensitive". However, we will discuss and present evidence to develop a novel hypothesis to suggest that while chronic increases in dietary salt intake do not elevate mean ABP in "non-salt-sensitive" animals, dietary salt intake does enhance several sympathetic reflexes thereby predisposing these animals and/or individuals to the development of salt-sensitive hypertension. Additional evidence raises an intriguing hypothesis that these enhanced sympathetic reflexes are largely attributed to the ability of excess dietary salt intake to selectively enhance the excitability of sympathetic-regulatory neurons in the rostral ventrolateral medulla. Insight into the cellular mechanisms by which dietary salt intake alters the responsiveness of RVLM circuits will likely provide a foundation for developing new therapeutic approaches to treat salt-sensitive hypertension. The paper represents an invited review by a symposium, award winner or keynote speaker at the Society for the Study of Ingestive Behavior [SSIB] Annual Meeting in Portland, July 2009.

Original languageEnglish (US)
Pages (from-to)519-524
Number of pages6
JournalPhysiology and Behavior
Volume100
Issue number5
DOIs
StatePublished - Jul 1 2010

Fingerprint

Salts
Arterial Pressure
Hypertension
Reflex
Aptitude
Vascular Resistance
Theoretical Models
Cardiovascular Diseases
Eating
Morbidity
Neurons
Mortality

All Science Journal Classification (ASJC) codes

  • Experimental and Cognitive Psychology
  • Behavioral Neuroscience

Cite this

Stocker, Sean D. ; Madden, Christopher J. ; Sved, Alan F. / Excess dietary salt intake alters the excitability of central sympathetic networks. In: Physiology and Behavior. 2010 ; Vol. 100, No. 5. pp. 519-524.
@article{7cd87baf17794e7389cf574a27f57322,
title = "Excess dietary salt intake alters the excitability of central sympathetic networks",
abstract = "The ingestion of excess dietary salt (defined as NaCl) is strongly correlated with cardiovascular disease, morbidity, mortality, and is regarded as a major contributing factor to the pathogenesis of hypertension. Although several mechanisms contribute to the adverse consequences of dietary salt intake, accumulating evidence suggests that dietary salt loading produces neurogenically-mediated increases in total peripheral resistance to raise arterial blood pressure (ABP). Evidence from clinical studies and experimental models clearly establishes a hypertensive effect of dietary salt loading in a subset of individuals who are deemed {"}salt-sensitive{"}. However, we will discuss and present evidence to develop a novel hypothesis to suggest that while chronic increases in dietary salt intake do not elevate mean ABP in {"}non-salt-sensitive{"} animals, dietary salt intake does enhance several sympathetic reflexes thereby predisposing these animals and/or individuals to the development of salt-sensitive hypertension. Additional evidence raises an intriguing hypothesis that these enhanced sympathetic reflexes are largely attributed to the ability of excess dietary salt intake to selectively enhance the excitability of sympathetic-regulatory neurons in the rostral ventrolateral medulla. Insight into the cellular mechanisms by which dietary salt intake alters the responsiveness of RVLM circuits will likely provide a foundation for developing new therapeutic approaches to treat salt-sensitive hypertension. The paper represents an invited review by a symposium, award winner or keynote speaker at the Society for the Study of Ingestive Behavior [SSIB] Annual Meeting in Portland, July 2009.",
author = "Stocker, {Sean D.} and Madden, {Christopher J.} and Sved, {Alan F.}",
year = "2010",
month = "7",
day = "1",
doi = "10.1016/j.physbeh.2010.04.024",
language = "English (US)",
volume = "100",
pages = "519--524",
journal = "Physiology and Behavior",
issn = "0031-9384",
publisher = "Elsevier Inc.",
number = "5",

}

Excess dietary salt intake alters the excitability of central sympathetic networks. / Stocker, Sean D.; Madden, Christopher J.; Sved, Alan F.

In: Physiology and Behavior, Vol. 100, No. 5, 01.07.2010, p. 519-524.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Excess dietary salt intake alters the excitability of central sympathetic networks

AU - Stocker, Sean D.

AU - Madden, Christopher J.

AU - Sved, Alan F.

PY - 2010/7/1

Y1 - 2010/7/1

N2 - The ingestion of excess dietary salt (defined as NaCl) is strongly correlated with cardiovascular disease, morbidity, mortality, and is regarded as a major contributing factor to the pathogenesis of hypertension. Although several mechanisms contribute to the adverse consequences of dietary salt intake, accumulating evidence suggests that dietary salt loading produces neurogenically-mediated increases in total peripheral resistance to raise arterial blood pressure (ABP). Evidence from clinical studies and experimental models clearly establishes a hypertensive effect of dietary salt loading in a subset of individuals who are deemed "salt-sensitive". However, we will discuss and present evidence to develop a novel hypothesis to suggest that while chronic increases in dietary salt intake do not elevate mean ABP in "non-salt-sensitive" animals, dietary salt intake does enhance several sympathetic reflexes thereby predisposing these animals and/or individuals to the development of salt-sensitive hypertension. Additional evidence raises an intriguing hypothesis that these enhanced sympathetic reflexes are largely attributed to the ability of excess dietary salt intake to selectively enhance the excitability of sympathetic-regulatory neurons in the rostral ventrolateral medulla. Insight into the cellular mechanisms by which dietary salt intake alters the responsiveness of RVLM circuits will likely provide a foundation for developing new therapeutic approaches to treat salt-sensitive hypertension. The paper represents an invited review by a symposium, award winner or keynote speaker at the Society for the Study of Ingestive Behavior [SSIB] Annual Meeting in Portland, July 2009.

AB - The ingestion of excess dietary salt (defined as NaCl) is strongly correlated with cardiovascular disease, morbidity, mortality, and is regarded as a major contributing factor to the pathogenesis of hypertension. Although several mechanisms contribute to the adverse consequences of dietary salt intake, accumulating evidence suggests that dietary salt loading produces neurogenically-mediated increases in total peripheral resistance to raise arterial blood pressure (ABP). Evidence from clinical studies and experimental models clearly establishes a hypertensive effect of dietary salt loading in a subset of individuals who are deemed "salt-sensitive". However, we will discuss and present evidence to develop a novel hypothesis to suggest that while chronic increases in dietary salt intake do not elevate mean ABP in "non-salt-sensitive" animals, dietary salt intake does enhance several sympathetic reflexes thereby predisposing these animals and/or individuals to the development of salt-sensitive hypertension. Additional evidence raises an intriguing hypothesis that these enhanced sympathetic reflexes are largely attributed to the ability of excess dietary salt intake to selectively enhance the excitability of sympathetic-regulatory neurons in the rostral ventrolateral medulla. Insight into the cellular mechanisms by which dietary salt intake alters the responsiveness of RVLM circuits will likely provide a foundation for developing new therapeutic approaches to treat salt-sensitive hypertension. The paper represents an invited review by a symposium, award winner or keynote speaker at the Society for the Study of Ingestive Behavior [SSIB] Annual Meeting in Portland, July 2009.

UR - http://www.scopus.com/inward/record.url?scp=77953698002&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=77953698002&partnerID=8YFLogxK

U2 - 10.1016/j.physbeh.2010.04.024

DO - 10.1016/j.physbeh.2010.04.024

M3 - Article

C2 - 20434471

AN - SCOPUS:77953698002

VL - 100

SP - 519

EP - 524

JO - Physiology and Behavior

JF - Physiology and Behavior

SN - 0031-9384

IS - 5

ER -