TY - JOUR
T1 - Anoxic contractions in isolated canine cerebral arteries
T2 - Contribution of endothelium-derived factors, metabolites of arachidonic acid, and calcium entry
AU - Katusic, Z. S.
AU - Vanhoutte, P. M.
N1 - Copyright:
Copyright 2018 Elsevier B.V., All rights reserved.
PY - 1986
Y1 - 1986
N2 - Experiments were designed to determine the role of the endothelial cells and the metabolism of arachidonic acid in anoxic contractions of isolated canine basilar arteries. Rings, with and without endothelium, of these arteries were suspended for isometric tension recording; anoxia was induced by switching the mixture gassing the organ chamber from 95% O2-5% CO2 to 95% N2-5% CO2. In rings with endothelium, anoxia evoked increases in tension under basal conditions and during contractions to 5-hydroxytryptamine, uridine triphosphate, prostaglandin F2α, and high K+. Under control conditions, these anoxic contractions were not prevented by α-adrenergic and serotonergic antagonists, by apyrase, or by inhibitors of cyclooxygenase. Anoxia prevented endothelium-dependent relaxations evoked by vasopressin and thrombin. In rings without endothelium, anoxia caused increases in tension during contractions evoked by various agonists, and in unstimulated preparations after inhibition of cyclooxygenase. Anoxic contractions were abolished by calcium entry blockers. These observations suggest that anoxic contractions of isolated canine basilar artery can be explained by the release of endothelium-derived contracting factor(s) and the accelerated entry of calcium in the smooth muscle cells, which possibly results from a diversion of arachidonic acid from the cyclooxygenase to the lipoxygenase pathway.
AB - Experiments were designed to determine the role of the endothelial cells and the metabolism of arachidonic acid in anoxic contractions of isolated canine basilar arteries. Rings, with and without endothelium, of these arteries were suspended for isometric tension recording; anoxia was induced by switching the mixture gassing the organ chamber from 95% O2-5% CO2 to 95% N2-5% CO2. In rings with endothelium, anoxia evoked increases in tension under basal conditions and during contractions to 5-hydroxytryptamine, uridine triphosphate, prostaglandin F2α, and high K+. Under control conditions, these anoxic contractions were not prevented by α-adrenergic and serotonergic antagonists, by apyrase, or by inhibitors of cyclooxygenase. Anoxia prevented endothelium-dependent relaxations evoked by vasopressin and thrombin. In rings without endothelium, anoxia caused increases in tension during contractions evoked by various agonists, and in unstimulated preparations after inhibition of cyclooxygenase. Anoxic contractions were abolished by calcium entry blockers. These observations suggest that anoxic contractions of isolated canine basilar artery can be explained by the release of endothelium-derived contracting factor(s) and the accelerated entry of calcium in the smooth muscle cells, which possibly results from a diversion of arachidonic acid from the cyclooxygenase to the lipoxygenase pathway.
KW - Calcium antagonists
KW - Thrombin
KW - Vascular smooth muscle
KW - Vasopressin
KW - Vasospasm
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U2 - 10.1097/00005344-198600088-00020
DO - 10.1097/00005344-198600088-00020
M3 - Article
C2 - 2433536
AN - SCOPUS:0022843938
SN - 0160-2446
VL - 8
SP - S97-S101
JO - Journal of Cardiovascular Pharmacology
JF - Journal of Cardiovascular Pharmacology
ER -