Document Detail


Dominance of flow-mediated constriction over flow-mediated dilatation in the rat carotid artery.
MedLine Citation:
PMID:  22537086     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND AND PURPOSE: The shearing forces generated by flow generally evoke dilatation in systemic vessels but constriction in the cerebral circulation. The aim of this study was to determine the effects of flow on the conduit artery delivering blood to the brain in the rat, that is, the carotid artery.
EXPERIMENTAL APPROACH: Carotid artery segments were mounted in a pressure myograph and pressurized to 100 mmHg. Changes in vessel diameter to flow (0.5-10 mL·min⁻¹ for 2-10 min) at constant pressure were then measured using a video dimension analyser.
KEY RESULTS: Following the induction of tone, the onset of flow evoked a transient dilatation followed by a powerful constriction that was sustained until the termination of flow. Endothelial denudation or treatment with indomethacin, N(G)-nitro-L-arginine methyl ester, or the combination of apamin and TRAM-34 showed that the initial flow-mediated dilatation arose from the combined actions of endothelium-derived NO and endothelium-derived hyperpolarizing factor (EDHF). The flow-mediated constriction, which increased in magnitude with increasing flow rate and duration of flow, was also endothelium dependent, but was unaffected by treatment with superoxide dismutase, BQ-123, indomethacin, HET0016 or carbenoxolone. Flow-mediated constriction therefore appeared not to involve superoxide anion, endothelin-1, a COX product, 20-HETE or gap-junctional communication.
CONCLUSIONS AND IMPLICATIONS: Although a weak, transient flow-mediated dilatation is observed in the rat carotid artery, the dominant response to flow is a powerful and sustained constriction. Whether this flow-mediated constriction in the carotid artery serves as an extracranial mechanism to regulate cerebral blood flow remains to be determined.
Authors:
John Craig; William Martin
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  British journal of pharmacology     Volume:  167     ISSN:  1476-5381     ISO Abbreviation:  Br. J. Pharmacol.     Publication Date:  2012 Oct 
Date Detail:
Created Date:  2012-09-05     Completed Date:  2013-01-17     Revised Date:  2013-10-13    
Medline Journal Info:
Nlm Unique ID:  7502536     Medline TA:  Br J Pharmacol     Country:  England    
Other Details:
Languages:  eng     Pagination:  527-36     Citation Subset:  IM    
Copyright Information:
© 2012 The Authors. British Journal of Pharmacology © 2012 The British Pharmacological Society.
Affiliation:
College of Medical, Veterinary and Life Sciences, West Medical Building, University of Glasgow, UK.
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MeSH Terms
Descriptor/Qualifier:
Animals
Biological Factors / metabolism
Carotid Arteries / drug effects,  metabolism*
Cerebrovascular Circulation / physiology
Female
Myography
Nitric Oxide / metabolism
Rats
Rats, Wistar
Regional Blood Flow / drug effects,  physiology*
Vasoconstriction / drug effects,  physiology*
Vasodilation / drug effects,  physiology*
Grant Support
ID/Acronym/Agency:
075682MA//Wellcome Trust
Chemical
Reg. No./Substance:
0/Biological Factors; 0/endothelium-dependent hyperpolarization factor; 10102-43-9/Nitric Oxide
Comments/Corrections

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