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Department of Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin 53226
Isolated rat middle cerebral arteries were
perfused and superfused with physiological salt solution equilibrated
with a control (~140 mmHg) or reduced (~35-40 mmHg)
PO2. In other experiments, cerebral
arteries were isolated and prostacyclin release was determined by
radioimmunoassay for 6-ketoprostaglandin F1
.
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 µM 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.
vascular smooth muscle; hypoxia; oxygen; adenosine 5'-triphosphate-sensitive potassium channels; endothelium
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