Electrical and mechanical responses of rat middle cerebral arteries to reduced PO2 and prostacyclin. Am J Physiol 1999 Feb;276(2):H509-16
Date
02/10/1999Pubmed ID
9950852DOI
10.1152/ajpheart.1999.276.2.H509Scopus ID
2-s2.0-0032984998 (requires institutional sign-in at Scopus site) 61 CitationsAbstract
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.
Author List
Lombard JH, Liu Y, Fredricks KT, Bizub DM, Roman RJ, Rusch NJMESH terms used to index this publication - Major topics in bold
AnimalsCerebral Arteries
Electrophysiology
Epoprostenol
Glyburide
Hypoxia
Iloprost
In Vitro Techniques
Male
Membrane Potentials
Muscle, Smooth, Vascular
Oxygen
Partial Pressure
Perfusion
Rats
Rats, Sprague-Dawley
Tetraethylammonium
Vasoconstriction
Vasodilation
Vasodilator Agents
