Document Detail


Alteration of endothelium-mediated vasodilator response in the rat hindlimb vasculature consecutive to chronic hypoxic stress: NO and EDHF involvement.
MedLine Citation:
PMID:  19520187     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The previously documented impairment of hindlimb blood flow consecutive to chronic hypoxia might be related to endothelial vasomotor dysfunction. The aim of this study was to assess in-vivo the effect of chronic hypoxic stress on endothelium-mediated vasodilator response of hindlimb vascular bed, especially as regards to endothelium-derived hyperpolarizing factor (EDHF) and nitric oxide (NO) pathway contribution. Dark Agouti rats were randomly assigned to live at barometric pressure approximately 760 mmHg (N rats) or approximately 550 mmHg (CH rats). Under anesthesia, catheters were placed in the carotid artery for arterial pressure measurement, and in the saphenous vein and iliac artery for drug delivery. Hindlimb blood flow (HBF) was measured by transit-time ultrasound flowmetry, at baseline and during endothelium-dependent vasodilator response induced by intra-arterial injection of acetylcholine (0.75 ng and 7.5 ng) with and without specific blockers of NOS (L-NAME) and EDHF (Charybdotoxin+Apamin). HBF and hindlimb vascular conductance changes in response to ACh infusion were significantly lower in CH than in N rats. The mechanisms responsible for this blunted response involved impairment in both NO pathway and EDHF. The chronic hypoxia-induced alteration of NO pathway was mainly related to the bioavailability of its substrate l-Arginine, since the infusion of l-Arginine restored the endothelial response to ACh in CH rats to the level of N rats. These results demonstrate that the impairment in endothelium-mediated vasodilator response of the hindlimb vascular tree induced by chronic hypoxic stress involves both NO and EDHF.
Authors:
C Reboul; A Gibault; S Tanguy; M Dauzat; P Obert
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Publication Detail:
Type:  Journal Article     Date:  2009-06-09
Journal Detail:
Title:  Vascular pharmacology     Volume:  51     ISSN:  1879-3649     ISO Abbreviation:  Vascul. Pharmacol.     Publication Date:    2009 Aug-Sep
Date Detail:
Created Date:  2009-08-11     Completed Date:  2009-10-30     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  101130615     Medline TA:  Vascul Pharmacol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  154-61     Citation Subset:  IM    
Affiliation:
EA4278, Research Laboratory: 'Physiology and physiopathology of Cardiovascular Adaptations to Exercise', Faculty of Sciences, Avignon University, Avignon, France. cyril.reboul@univ-avignon.fr
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MeSH Terms
Descriptor/Qualifier:
Acetylcholine / physiology
Animals
Arginine / physiology
Atmosphere Exposure Chambers
Biological Factors / antagonists & inhibitors,  physiology*
Blood Pressure
Diet
Endothelium, Vascular / physiology*
Hindlimb / blood supply
Infusions, Intravenous
Male
Nitric Oxide / physiology*
Nitric Oxide Synthase / antagonists & inhibitors
Oxygen / physiology*
Random Allocation
Rats
Regional Blood Flow
Stress, Physiological*
Time Factors
Vasodilation / physiology*
Chemical
Reg. No./Substance:
0/Biological Factors; 0/endothelium-dependent hyperpolarization factor; 10102-43-9/Nitric Oxide; 51-84-3/Acetylcholine; 74-79-3/Arginine; 7782-44-7/Oxygen; EC 1.14.13.39/Nitric Oxide Synthase

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


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