Document Detail


Functional sympatholysis is impaired in hypertensive humans.
MedLine Citation:
PMID:  21224235     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
In healthy individuals, sympathetic vasoconstriction is markedly blunted in exercising muscles to optimize blood flow to the metabolically active muscle fibres. This protective mechanism, termed functional sympatholysis, is impaired in rat models of angiotensin-dependent hypertension. However, the relevance of these findings to human hypertension is unknown. Therefore, in 13 hypertensive and 17 normotensive subjects we measured muscle oxygenation and forearm blood flow (FBF) responses to reflex increases in sympathetic nerve activity (SNA) evoked by lower body negative pressure (LBNP) at rest and during moderate-intensity rhythmic handgrip exercise. In the normotensives, LBNP caused decreases in oxygenation and FBF (−16 ± 2% and −23 ± 4%, respectively) in resting forearm but not in exercising forearm (−1 ± 2% and −1 ± 3%, respectively; P < 0.05 vs. rest). In the hypertensives, LBNP evoked decreases in oxygenation and FBF that were similar in the resting and exercising forearm (−14 ± 2% vs. −12 ± 2% and −20 ± 3% vs. −13 ± 2%, respectively; P > 0.05), indicating impaired functional sympatholysis. In the hypertensives, SNA was unexpectedly increased by 54 ± 11% during handgrip alone. However, when SNA was experimentally increased during exercise in the normotensives, sympatholysis was unaffected. Treatment for 4 weeks with the angiotensin receptor blocker irbesartan, but not with the thiazide-type diuretic chlorthalidone, restored sympatholysis in the hypertensives. These data provide the first evidence that functional sympatholysis is impaired in hypertensive humans by a mechanism that appears to involve an angiotensin-dependent increase in sympathetic vasoconstriction in the exercising muscles.
Authors:
Wanpen Vongpatanasin; Zhongyun Wang; Debbie Arbique; Gary Arbique; Beverley Adams-Huet; Jere H Mitchell; Ronald G Victor; Gail D Thomas
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2011-01-04
Journal Detail:
Title:  The Journal of physiology     Volume:  589     ISSN:  1469-7793     ISO Abbreviation:  J. Physiol. (Lond.)     Publication Date:  2011 Mar 
Date Detail:
Created Date:  2011-04-13     Completed Date:  2011-08-15     Revised Date:  2013-07-02    
Medline Journal Info:
Nlm Unique ID:  0266262     Medline TA:  J Physiol     Country:  England    
Other Details:
Languages:  eng     Pagination:  1209-20     Citation Subset:  IM    
Affiliation:
Hypertension Section, Cardiology Division, University of Texas Southwestern Medical Center, 5323 Harry Hines Blvd., U9.400, Dallas, TX 75390-8586, USA. wanpen.vongpatanasin@utsouthwestern.edu
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MeSH Terms
Descriptor/Qualifier:
Adult
Angiotensin II Type 1 Receptor Blockers / pharmacology
Biphenyl Compounds / pharmacology
Blood Pressure / drug effects,  physiology*
Electrocardiography
Female
Forearm / blood supply*
Hand Strength / physiology
Heart Rate / drug effects,  physiology
Humans
Hypertension / physiopathology*
Lower Body Negative Pressure
Male
Middle Aged
Muscle Contraction / physiology
Muscle, Skeletal / blood supply,  drug effects,  physiopathology
Oxygen Consumption / drug effects,  physiology*
Regional Blood Flow / drug effects,  physiology*
Sympathetic Nervous System / drug effects,  physiopathology*
Tetrazoles / pharmacology
Vasoconstriction / drug effects,  physiology
Grant Support
ID/Acronym/Agency:
R01 HL-078782/HL/NHLBI NIH HHS; UL1RR-024982/RR/NCRR NIH HHS
Chemical
Reg. No./Substance:
0/Angiotensin II Type 1 Receptor Blockers; 0/Biphenyl Compounds; 0/Tetrazoles; 138402-11-6/irbesartan
Comments/Corrections

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


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