Journal article
TRANSLATION OF SALT RETENTION TO CENTRAL ACTIVATION OF THE SYMPATHETIC NERVOUS SYSTEM IN HYPERTENSION
Clinical and experimental pharmacology & physiology, Vol.32(5-6), pp.426-432
Received 8 December 2004; revision 29 December 2004; accepted 13 January 2005.
05/2005
DOI: 10.1111/j.1440-1681.2005.04206.x
PMID: 15854153
Abstract
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. It is proposed that increased salt intake causes salt retention and raises plasma sodium chloride (NaCl) concentrations, which activate sodiutn/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. 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.
Details
- Title: Subtitle
- TRANSLATION OF SALT RETENTION TO CENTRAL ACTIVATION OF THE SYMPATHETIC NERVOUS SYSTEM IN HYPERTENSION
- Creators
- Virginia L Brooks - Department of Physiology and Pharmacology, Oregon Health & Science University, Portland, OregonJoseph R Haywood - Department of Pharmacology and Toxicology, Michigan State University, East Lansing, Michigan andAlan Kim Johnson - Departments of Psychology, Pharmacology and Exercise Science, University of Iowa, Iowa City, Iowa, USA
- Resource Type
- Journal article
- Publication Details
- Clinical and experimental pharmacology & physiology, Vol.32(5-6), pp.426-432
- Edition
- Received 8 December 2004; revision 29 December 2004; accepted 13 January 2005.
- Publisher
- Blackwell Science, Ltd
- DOI
- 10.1111/j.1440-1681.2005.04206.x
- PMID
- 15854153
- ISSN
- 0305-1870
- eISSN
- 1440-1681
- Number of pages
- 7
- Language
- English
- Date published
- 05/2005
- Academic Unit
- Psychological and Brain Sciences; Neuroscience and Pharmacology; Health and Human Physiology
- Record Identifier
- 9984214758202771
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