Document Detail


Sympathoexcitation by oxidative stress in the brain mediates arterial pressure elevation in salt-sensitive hypertension.
MedLine Citation:
PMID:  17576857     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Central sympathoexcitation is involved in the pathogenesis of salt-sensitive hypertension. We have suggested that oxidative stress in the brain modulates the sympathetic regulation of arterial pressure. Thus, we investigated whether oxidative stress could mediate central sympathoexcitation in salt-sensitive hypertension. Five- to 6-week-old male Dahl salt-sensitive rats and salt-resistant rats were fed with a normal (0.3%) or high- (8%) salt diet for 4 weeks. In urethane-anesthetized and artificially ventilated rats, arterial pressure, renal sympathetic nerve activity, and heart rate decreased in a dose-dependent fashion, when 20 or 40 micromol of tempol, a membrane-permeable superoxide dismutase mimetic, was infused into the lateral cerebral ventricle. The same degree of reduction was noted in salt-sensitive and salt-resistant rats without salt loading. Salt loading significantly increased central tempol-induced reductions in arterial pressure (-29.1+/-4.8% versus -10.6+/-3.3% at 40 micromol; P<0.01), sympathetic nerve activity (-18.7+/-2.0% versus -7.1+/-1.8%; P<0.01), and heart rate (-10.7+/-2.8% versus -2.0+/-0.7%; P<0.05) in salt-sensitive rats but not in salt-resistant rats. Intracerebroventricular diphenyleneiodonium, a reduced nicotinamide-adenine dinucleotide phosphate oxidase inhibitor, also elicited significantly greater reduction in each parameter in salt-loaded salt-sensitive rats. Moreover, salt loading increased reduced nicotinamide-adenine dinucleotide phosphate-dependent superoxide production in the hypothalamus in salt-sensitive rats but not in salt-resistant rats. In addition, reduced nicotinamide-adenine dinucleotide phosphate oxidase subunits p22(phox), p47(phox), and gp91(phox) mRNA expression significantly increased in the hypothalamus of salt-loaded salt-sensitive rats. In conclusion, in salt-sensitive hypertension, increased oxidative stress in the brain, possibly via activation of reduced nicotinamide-adenine dinucleotide phosphate oxidase, may elevate arterial pressure through central sympathoexcitation.
Authors:
Megumi Fujita; Katsuyuki Ando; Ai Nagae; Toshiro Fujita
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2007-06-18
Journal Detail:
Title:  Hypertension     Volume:  50     ISSN:  1524-4563     ISO Abbreviation:  Hypertension     Publication Date:  2007 Aug 
Date Detail:
Created Date:  2007-07-19     Completed Date:  2007-08-08     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  7906255     Medline TA:  Hypertension     Country:  United States    
Other Details:
Languages:  eng     Pagination:  360-7     Citation Subset:  IM    
Affiliation:
Department of Nephrology and Endocrinology, Faculty of Medicine, University of Tokyo, 7-3-1, Hongo, Bunkyo-ku, Tokyo, 113-8655, Japan.
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MeSH Terms
Descriptor/Qualifier:
Analysis of Variance
Animals
Blood Pressure / drug effects
Hypertension / etiology*,  physiopathology
Hypothalamus / drug effects,  physiology
Male
NADP / pharmacology
Oxidative Stress
Probability
Random Allocation
Rats
Rats, Inbred Dahl
Rats, Wistar
Reactive Oxygen Species / adverse effects*
Reference Values
Reverse Transcriptase Polymerase Chain Reaction
Risk Factors
Sensitivity and Specificity
Sodium Chloride / pharmacology*
Superoxides / metabolism
Sympathetic Nervous System / drug effects*,  physiology
Chemical
Reg. No./Substance:
0/Reactive Oxygen Species; 11062-77-4/Superoxides; 53-59-8/NADP; 7647-14-5/Sodium Chloride

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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