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TRANSLATION OF SALT RETENTION TO CENTRAL ACTIVATION OF THE SYMPATHETIC NERVOUS SYSTEM IN HYPERTENSION
Author(s) -
Brooks Virginia L,
Haywood Joseph R,
Johnson Alan Kim
Publication year - 2005
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/j.1440-1681.2005.04206.x
Subject(s) - sympathetic nervous system , endocrinology , medicine , osmoreceptor , sodium , blood pressure , renin–angiotensin system , aldosterone , tonicity , angiotensin ii , central nervous system , thirst , chemistry , organic chemistry
SUMMARY 1. Increased dietary salt increases blood pressure in many hypertensive individuals, producing salt‐sensitive hypertension (SSH). The cause is unknown, but a major component appears to be activation of the sympathetic nervous system. The purpose of this short review is to present one hypothesis to explain how increased dietary salt increases sympathetic activity in SSH. 2. It is proposed that increased salt intake causes salt retention and raises plasma sodium chloride (NaCl) concentrations, which activate sodium/osmoreceptors to trigger sympathoexcitation. Moreover, we suggest that small and often undetectable increases in osmolality can drive significant sympathoexcitation, because the gain of the relationship between osmolality and increased sympathetic activity is enhanced. Multiple factors may contribute to this facilitation, including inappropriately elevated levels of angiotensin II or aldosterone, changes in gene expression or synaptic plasticity and increased sodium concentrations in cerebrospinal fluid. 3. Future studies are required to delineate the brain sites and mechanisms of action and interaction of osmolality and these amplification factors to elicit sustained sympathoexcitation in SSH.