Document Detail


Electrical and mechanical responses of rat middle cerebral arteries to reduced PO2 and prostacyclin.
MedLine Citation:
PMID:  9950852     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Isolated rat middle cerebral arteries were perfused and superfused with physiological salt solution equilibrated with a control (approximately 140 mmHg) or reduced (approximately 35-40 mmHg) PO2. In other experiments, cerebral arteries were isolated and prostacyclin release was determined by radioimmunoassay for 6-ketoprostaglandin F1alpha. Equilibration of the vessels with reduced PO2 (35 mmHg) solution caused a significant increase in prostacyclin release relative to control PO2 (140 mmHg) conditions. Exposure of middle cerebral arteries to reduced PO2 caused vascular smooth muscle (VSM) hyperpolarization and vessel relaxation, which could be blocked by 1 microM glibenclamide, an inhibitor of the ATP-sensitive K+ channel, but not by 1 mM tetraethylammonium (TEA), an inhibitor of the Ca2+-activated K+ channel. Glibenclamide also inhibited VSM hyperpolarization and vasodilation in response to the stable prostacyclin analog iloprost, but TEA did not affect iloprost-induced dilation of the vessel. Endothelial removal eliminated the electrical and mechanical responses of the arteries to reduced PO2, but vessel responses to iloprost were similar to those of intact vessels. The results of this study are consistent with the hypothesis that hypoxic dilation of rat middle cerebral arteries is due to VSM hyperpolarization mediated by prostacyclin-induced activation of glibenclamide-sensitive K+ channels.
Authors:
J H Lombard; Y Liu; K T Fredricks; D M Bizub; R J Roman; N J Rusch
Publication Detail:
Type:  In Vitro; Journal Article; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  The American journal of physiology     Volume:  276     ISSN:  0002-9513     ISO Abbreviation:  Am. J. Physiol.     Publication Date:  1999 Feb 
Date Detail:
Created Date:  1999-03-30     Completed Date:  1999-03-30     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  0370511     Medline TA:  Am J Physiol     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  H509-16     Citation Subset:  IM    
Affiliation:
Department of Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin 53226, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Anoxia / physiopathology
Cerebral Arteries / drug effects,  physiology*
Electrophysiology
Epoprostenol / metabolism*
Glyburide / pharmacology
Iloprost / pharmacology
Male
Membrane Potentials / physiology
Muscle, Smooth, Vascular / physiology
Oxygen / metabolism*
Partial Pressure
Perfusion
Rats
Rats, Sprague-Dawley
Tetraethylammonium / pharmacology
Vasoconstriction / physiology*
Vasodilation / physiology
Vasodilator Agents / pharmacology
Grant Support
ID/Acronym/Agency:
HL-29587/HL/NHLBI NIH HHS; HL-37374/HL/NHLBI NIH HHS; HL-52211/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Vasodilator Agents; 10238-21-8/Glyburide; 35121-78-9/Epoprostenol; 66-40-0/Tetraethylammonium; 7782-44-7/Oxygen; 78919-13-8/Iloprost

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


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