Document Detail


Nitric oxide-mediated vasodilation becomes independent of beta-adrenergic receptor activation with increased intensity of hypoxic exercise.
MedLine Citation:
PMID:  21193565     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Hypoxic vasodilation in skeletal muscle at rest is known to include β-adrenergic receptor-stimulated nitric oxide (NO) release. We previously reported that the augmented skeletal muscle vasodilation during mild hypoxic forearm exercise includes β-adrenergic mechanisms. However, it is unclear whether a β-adrenergic receptor-stimulated NO component exists during hypoxic exercise. We hypothesized that NO-mediated vasodilation becomes independent of β-adrenergic receptor activation with increased exercise intensity during hypoxic exercise. Ten subjects (7 men, 3 women; 23 ± 1 yr) breathed hypoxic gas to titrate arterial O(2) saturation to 80% while remaining normocapnic. Subjects performed two consecutive bouts of incremental rhythmic forearm exercise (10% and 20% of maximum) with local administration (via a brachial artery catheter) of propranolol (β-adrenergic receptor inhibition) alone and with the combination of propranolol and nitric oxide synthase inhibition [N(G)-monomethyl-l-arginine (l-NMMA)] under normoxic and hypoxic conditions. Forearm blood flow (FBF, ml/min; Doppler ultrasound) and blood pressure [mean arterial pressure (MAP), mmHg; brachial artery catheter] were assessed, and forearm vascular conductance (FVC, ml·min(-1)·100 mmHg(-1)) was calculated (FBF/MAP). During propranolol alone, the rise in FVC (Δ from normoxic baseline) due to hypoxic exercise was 217 ± 29 and 415 ± 41 ml·min(-1)·100 mmHg(-1) (10% and 20% of maximum, respectively). Combined propranolol-l-NMMA infusion during hypoxic exercise attenuated ΔFVC at 20% (352 ± 44 ml·min(-1)·100 mmHg(-1); P < 0.001) but not at 10% (202 ± 28 ml·min(-1)·100 mmHg(-1); P = 0.08) of maximum compared with propranolol alone. These data, when integrated with earlier findings, demonstrate that NO contributes to the compensatory vasodilation during mild and moderate hypoxic exercise; a β-adrenergic receptor-stimulated NO component exists during low-intensity hypoxic exercise. However, the source of the NO becomes less dependent on β-adrenergic mechanisms as exercise intensity increases.
Authors:
Darren P Casey; Timothy B Curry; Brad W Wilkins; Michael J Joyner
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2010-12-30
Journal Detail:
Title:  Journal of applied physiology (Bethesda, Md. : 1985)     Volume:  110     ISSN:  1522-1601     ISO Abbreviation:  J. Appl. Physiol.     Publication Date:  2011 Mar 
Date Detail:
Created Date:  2011-03-09     Completed Date:  2011-07-07     Revised Date:  2012-03-01    
Medline Journal Info:
Nlm Unique ID:  8502536     Medline TA:  J Appl Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  687-94     Citation Subset:  IM    
Affiliation:
Dept. of Anesthesiology, Mayo Clinic, 200 First St. SW, Rochester, MN 55905, USA. casey.darren@mayo.edu
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MeSH Terms
Descriptor/Qualifier:
Anoxia / physiopathology*
Female
Humans
Male
Nitric Oxide / blood*
Physical Exertion*
Receptors, Adrenergic, beta / metabolism*
Vasodilation*
Young Adult
Grant Support
ID/Acronym/Agency:
AR-55819/AR/NIAMS NIH HHS; HL-46493/HL/NHLBI NIH HHS; RR-024150/RR/NCRR NIH HHS
Chemical
Reg. No./Substance:
0/Receptors, Adrenergic, beta; 10102-43-9/Nitric Oxide

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


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