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pubmed-article:1504730pubmed:abstractText1. The aim of this study was to investigate whether the hypotensive effect of rat alpha-calcitonin gene-related peptide (alpha CGRP) in conscious rats is mediated by endothelium-derived nitric oxide (NO) or the opening of adenosine 5'-triphosphate (ATP)-sensitive potassium (KATP) channels. 2. Dose-mean arterial pressure (MAP)-response curves of alpha CGRP were examined in the presence of vehicle, phenylephrine, KATP channel antagonist glibenclamide or NO synthase inhibitors, NG-nitro-L-arginine methyl ester (L-NAME) and NG-nitro-D-arginine methyl ester (D-NAME). Dose-MAP-response curves for sodium nitroprusside were also constructed in the presence and absence of L-NAME and D-NAME. 3. alpha CGRP and nitroprusside produced dose-dependent reductions in MAP which were potentiated by phenylephrine. Both L-NAME and D-NAME attenuated the depressor response to alpha CGRP but not nitroprusside. 4. Dose-MAP-response curves for pinacidil, a KATP-channel activator, were also examined in the presence of glibenclamide or vehicle. Glibenclamide attenuated pinacidil- but not alpha CGRP-induced reductions in MAP. 5. It is concluded that the hypotensive effects of alpha CGRP are partially mediated via endothelium-derived NO but not via the opening of KATP channels.lld:pubmed
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pubmed-article:1504730pubmed:authorpubmed-author:MELOM JMJlld:pubmed
pubmed-article:1504730pubmed:authorpubmed-author:ChangS DSDlld:pubmed
pubmed-article:1504730pubmed:authorpubmed-author:WangY XYXlld:pubmed
pubmed-article:1504730pubmed:authorpubmed-author:AbdelrahmanAAlld:pubmed
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pubmed-article:1504730pubmed:articleTitleMechanism of the vasodilator action of calcitonin gene-related peptide in conscious rats.lld:pubmed
pubmed-article:1504730pubmed:affiliationDepartment of Pharmacology & Therapeutics, Faculty of Medicine, University of British Columbia, Vancouver, Canada.lld:pubmed
pubmed-article:1504730pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:1504730pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
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