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- Publisher Website: 10.1097/00005344-198600088-00020
- Scopus: eid_2-s2.0-0022843938
- PMID: 2433536
- WOS: WOS:A1986F518100020
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Article: Anoxic contractions in isolated canine cerebral arteries: Contribution of endothelium-derived factors, metabolites of arachidonic acid, and calcium entry
Title | Anoxic contractions in isolated canine cerebral arteries: Contribution of endothelium-derived factors, metabolites of arachidonic acid, and calcium entry |
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Authors | |
Keywords | Calcium antagonists Thrombin Vascular smooth muscle Vasopressin Vasospasm |
Issue Date | 1986 |
Publisher | Lippincott Williams & Wilkins. The Journal's web site is located at http://www.cardiovascularpharm.com/ |
Citation | Journal Of Cardiovascular Pharmacology, 1986, v. 8 SUPPL.8, p. S97-S101 How to Cite? |
Abstract | 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 F(2α), 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. |
Persistent Identifier | http://hdl.handle.net/10722/170824 |
ISSN | 2023 Impact Factor: 2.6 2023 SCImago Journal Rankings: 0.610 |
ISI Accession Number ID |
DC Field | Value | Language |
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dc.contributor.author | Katusic, ZS | en_US |
dc.contributor.author | Vanhoutte, PM | en_US |
dc.date.accessioned | 2012-10-30T06:11:01Z | - |
dc.date.available | 2012-10-30T06:11:01Z | - |
dc.date.issued | 1986 | en_US |
dc.identifier.citation | Journal Of Cardiovascular Pharmacology, 1986, v. 8 SUPPL.8, p. S97-S101 | en_US |
dc.identifier.issn | 0160-2446 | en_US |
dc.identifier.uri | http://hdl.handle.net/10722/170824 | - |
dc.description.abstract | 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 F(2α), 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. | en_US |
dc.language | eng | en_US |
dc.publisher | Lippincott Williams & Wilkins. The Journal's web site is located at http://www.cardiovascularpharm.com/ | en_US |
dc.relation.ispartof | Journal of Cardiovascular Pharmacology | en_US |
dc.subject | Calcium antagonists | - |
dc.subject | Thrombin | - |
dc.subject | Vascular smooth muscle | - |
dc.subject | Vasopressin | - |
dc.subject | Vasospasm | - |
dc.subject.mesh | Animals | en_US |
dc.subject.mesh | Anoxia - Physiopathology | en_US |
dc.subject.mesh | Arachidonic Acid | en_US |
dc.subject.mesh | Arachidonic Acids - Metabolism | en_US |
dc.subject.mesh | Calcium - Metabolism | en_US |
dc.subject.mesh | Cerebral Arteries - Physiopathology | en_US |
dc.subject.mesh | Cyclooxygenase Inhibitors | en_US |
dc.subject.mesh | Diltiazem - Pharmacology | en_US |
dc.subject.mesh | Dinoprost | en_US |
dc.subject.mesh | Dogs | en_US |
dc.subject.mesh | Endothelium - Analysis | en_US |
dc.subject.mesh | Female | en_US |
dc.subject.mesh | Male | en_US |
dc.subject.mesh | Potassium - Pharmacology | en_US |
dc.subject.mesh | Prostaglandins F - Pharmacology | en_US |
dc.subject.mesh | Serotonin - Pharmacology | en_US |
dc.subject.mesh | Uridine Triphosphate - Pharmacology | en_US |
dc.subject.mesh | Vasoconstriction | en_US |
dc.title | Anoxic contractions in isolated canine cerebral arteries: Contribution of endothelium-derived factors, metabolites of arachidonic acid, and calcium entry | en_US |
dc.type | Article | en_US |
dc.identifier.email | Vanhoutte, PM:vanhoutt@hku.hk | en_US |
dc.identifier.authority | Vanhoutte, PM=rp00238 | en_US |
dc.description.nature | link_to_subscribed_fulltext | en_US |
dc.identifier.doi | 10.1097/00005344-198600088-00020 | - |
dc.identifier.pmid | 2433536 | - |
dc.identifier.scopus | eid_2-s2.0-0022843938 | en_US |
dc.identifier.volume | 8 | en_US |
dc.identifier.issue | SUPPL.8 | en_US |
dc.identifier.spage | S97 | en_US |
dc.identifier.epage | S101 | en_US |
dc.identifier.isi | WOS:A1986F518100020 | - |
dc.publisher.place | United States | en_US |
dc.identifier.scopusauthorid | Katusic, ZS=7006971465 | en_US |
dc.identifier.scopusauthorid | Vanhoutte, PM=7202304247 | en_US |
dc.identifier.issnl | 0160-2446 | - |