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Article: Amplification of alpha adrenergic vasoconstriction in canine isolated mesenteric artery and vein

TitleAmplification of alpha adrenergic vasoconstriction in canine isolated mesenteric artery and vein
Authors
Issue Date1992
PublisherAmerican Society for Pharmacology and Experimental Therapeutics. The Journal's web site is located at http://jpet.aspetjournals.org
Citation
Journal Of Pharmacology And Experimental Therapeutics, 1992, v. 260 n. 3, p. 1119-1127 How to Cite?
AbstractThe interactions between UK-14304 and other vasoconstrictor agents were investigated using isolated canine mesenteric vascular rings mounted in tissue baths for the measurement of isometric contraction. In the mesenteric artery, exposure to UK-14304 caused a small contraction, producing 8% of the KCl maximal response. In the presence of either 20 mM KCl or 10-9 M endothelin-1, which had small contractile effects, UK-14304 produced a biphasic concentration-response curve; 10-7 M rauwolscine inhibited the responses to low concentrations of UK-14304 and 10-7 M prazosin blocked the responses to high concentrations of UK-14304. In the presence of 10-8 M Bay K 8644, UK-14304 elicited a monophasic concentration-dependent contraction that was antagonized by 10-7 M prazosin, not by 10-7 M rauwolscine. In the mesenteric vein, UK-14304 elicited concentration-dependent contractions, producing 63% of the KCl maximal response. The lower part of the biphasic concentration-response curve was inhibited by 10-7 M rauwolscine and the upper part of the curve was antagonized by 10-7 M prazosin. The presence in the medium of 20 mM KCl, 10-11 M endothelin-1 or 10-9 M Bay K 8644, which increased resting tension less than 10% of the KCl maximal response, markedly enhanced the responses to UK-14304 primarily at concentrations lower than 10-6 M. The enhancement of responses were prazosin (10-7 M)- resistant and rauwolscine (10-7 M)-sensitive. In canine mesenteric artery, our data suggest that addition of threshold concentrations of either KCl or endothelin-1 enhanced UK-14304 response via amplification of both postjunctional alpha1 and alpha2 adrenoceptor-mediated responses, while the potentiating effect of Bay K 8644 may only result from amplification of postjunctional alpha1 adrenoceptor-mediated responses. In canine mesenteric vein, either KCl, endothelin-1 or Bay K 8644 enhanced the contractile response to UK-14304 through amplification of postjunctional alpha2 adrenoceptor-mediated responses.
Persistent Identifierhttp://hdl.handle.net/10722/171570
ISSN
2015 Impact Factor: 3.76
2015 SCImago Journal Rankings: 1.847
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorShimamoto, Hen_US
dc.contributor.authorBourreau, JPen_US
dc.contributor.authorKwan, CYen_US
dc.contributor.authorDaniel, EEen_US
dc.date.accessioned2012-10-30T06:15:44Z-
dc.date.available2012-10-30T06:15:44Z-
dc.date.issued1992en_US
dc.identifier.citationJournal Of Pharmacology And Experimental Therapeutics, 1992, v. 260 n. 3, p. 1119-1127en_US
dc.identifier.issn0022-3565en_US
dc.identifier.urihttp://hdl.handle.net/10722/171570-
dc.description.abstractThe interactions between UK-14304 and other vasoconstrictor agents were investigated using isolated canine mesenteric vascular rings mounted in tissue baths for the measurement of isometric contraction. In the mesenteric artery, exposure to UK-14304 caused a small contraction, producing 8% of the KCl maximal response. In the presence of either 20 mM KCl or 10-9 M endothelin-1, which had small contractile effects, UK-14304 produced a biphasic concentration-response curve; 10-7 M rauwolscine inhibited the responses to low concentrations of UK-14304 and 10-7 M prazosin blocked the responses to high concentrations of UK-14304. In the presence of 10-8 M Bay K 8644, UK-14304 elicited a monophasic concentration-dependent contraction that was antagonized by 10-7 M prazosin, not by 10-7 M rauwolscine. In the mesenteric vein, UK-14304 elicited concentration-dependent contractions, producing 63% of the KCl maximal response. The lower part of the biphasic concentration-response curve was inhibited by 10-7 M rauwolscine and the upper part of the curve was antagonized by 10-7 M prazosin. The presence in the medium of 20 mM KCl, 10-11 M endothelin-1 or 10-9 M Bay K 8644, which increased resting tension less than 10% of the KCl maximal response, markedly enhanced the responses to UK-14304 primarily at concentrations lower than 10-6 M. The enhancement of responses were prazosin (10-7 M)- resistant and rauwolscine (10-7 M)-sensitive. In canine mesenteric artery, our data suggest that addition of threshold concentrations of either KCl or endothelin-1 enhanced UK-14304 response via amplification of both postjunctional alpha1 and alpha2 adrenoceptor-mediated responses, while the potentiating effect of Bay K 8644 may only result from amplification of postjunctional alpha1 adrenoceptor-mediated responses. In canine mesenteric vein, either KCl, endothelin-1 or Bay K 8644 enhanced the contractile response to UK-14304 through amplification of postjunctional alpha2 adrenoceptor-mediated responses.en_US
dc.languageengen_US
dc.publisherAmerican Society for Pharmacology and Experimental Therapeutics. The Journal's web site is located at http://jpet.aspetjournals.orgen_US
dc.relation.ispartofJournal of Pharmacology and Experimental Therapeuticsen_US
dc.subject.mesh3-Pyridinecarboxylic Acid, 1,4-Dihydro-2,6-Dimethyl-5-Nitro-4-(2-(Trifluoromethyl)Phenyl)-, Methyl Ester - Pharmacologyen_US
dc.subject.meshAdrenergic Alpha-Agonists - Pharmacologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshCalcium - Metabolismen_US
dc.subject.meshDogsen_US
dc.subject.meshDose-Response Relationship, Drugen_US
dc.subject.meshEndothelins - Pharmacologyen_US
dc.subject.meshFemaleen_US
dc.subject.meshMaleen_US
dc.subject.meshMesenteric Arteries - Drug Effects - Physiologyen_US
dc.subject.meshMesenteric Veins - Drug Effects - Physiologyen_US
dc.subject.meshPotassium Chloride - Pharmacologyen_US
dc.subject.meshPrazosin - Pharmacologyen_US
dc.subject.meshQuinoxalines - Pharmacologyen_US
dc.subject.meshReceptors, Adrenergic, Alpha - Physiologyen_US
dc.subject.meshVasoconstriction - Drug Effectsen_US
dc.titleAmplification of alpha adrenergic vasoconstriction in canine isolated mesenteric artery and veinen_US
dc.typeArticleen_US
dc.identifier.emailBourreau, JP:bourreau@hkucc.hku.hken_US
dc.identifier.authorityBourreau, JP=rp00389en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.pmid1372048-
dc.identifier.scopuseid_2-s2.0-0026643638en_US
dc.identifier.volume260en_US
dc.identifier.issue3en_US
dc.identifier.spage1119en_US
dc.identifier.epage1127en_US
dc.identifier.isiWOS:A1992HJ01900026-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridShimamoto, H=7006565682en_US
dc.identifier.scopusauthoridBourreau, JP=7003927886en_US
dc.identifier.scopusauthoridKwan, CY=7201421224en_US
dc.identifier.scopusauthoridDaniel, EE=35474017600en_US

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