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Physiol Behav. 2010 Jul 14;100(5):519-24. doi: 10.1016/j.physbeh.2010.04.024. Epub 2010 May 1.

Excess dietary salt intake alters the excitability of central sympathetic networks.

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  • 1Department of Cellular & Molecular Physiology, Penn State University College of Medicine, 500 University Drive H166, Hershey, PA 17033, USA. sstocker@hmc.psu.edu

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.

2010 Elsevier Inc. All rights reserved.

PMID:
20434471
[PubMed - indexed for MEDLINE]
PMCID:
PMC3024145
Free PMC Article

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