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Article: Alpha-1 adrenoceptors and calcium in isolated canine coronary arteries

TitleAlpha-1 adrenoceptors and calcium in isolated canine coronary arteries
Authors
Issue Date1983
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, 1983, v. 226 n. 3, p. 668-672 How to Cite?
AbstractExperiments were designed to define the postjunctional alpha adrenoceptor subtype(s) in large canine coronary arteries and to determine the dependency of contractions due to their activation upon the entry of extracellular calcium. Rings of left circumflex coronary artery were mounted at their optimal length for isometric tension recording in organ chambers filled with physiological salt solution. Phenylephrine and cirazoline were full agonists relative to norepinephrine. Methoxamine was a partial agonist relative to norepinephrine whereas clonidine, xylazine, B-HT 920 and B-HT 933 produced minimal contractions. Prazosin competitively inhibited the contractile response to phenylephrine (pA2 = 8.6), whereas rauwolscine caused a noncompetitive inhibition and was more than 100 times less potent than prazosin at inhibiting the response to phenylephrine. Similar results were obtained using norepinephrine (in the presence of propranolol) as the agonist. The calcium-entry blockers nimodipine, verapamil and diltiazem inhibited contractions caused by norepinephrine, phenylephrine and cirazoline. Removal of extracellular calcium abolished the response to cirazoline. These results suggest that in large canine coronary arteries: 1) only alpha-1 adrenoceptors are present postjunctionally and 2) responses due to alpha-1 adrenoceptor activation are dependent upon extracellular calcium.
Persistent Identifierhttp://hdl.handle.net/10722/170689
ISSN
2015 Impact Factor: 3.76
2015 SCImago Journal Rankings: 1.847
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorRimele, TJen_US
dc.contributor.authorRooke, TWen_US
dc.contributor.authorAarhus, LLen_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:10:27Z-
dc.date.available2012-10-30T06:10:27Z-
dc.date.issued1983en_US
dc.identifier.citationJournal Of Pharmacology And Experimental Therapeutics, 1983, v. 226 n. 3, p. 668-672en_US
dc.identifier.issn0022-3565en_US
dc.identifier.urihttp://hdl.handle.net/10722/170689-
dc.description.abstractExperiments were designed to define the postjunctional alpha adrenoceptor subtype(s) in large canine coronary arteries and to determine the dependency of contractions due to their activation upon the entry of extracellular calcium. Rings of left circumflex coronary artery were mounted at their optimal length for isometric tension recording in organ chambers filled with physiological salt solution. Phenylephrine and cirazoline were full agonists relative to norepinephrine. Methoxamine was a partial agonist relative to norepinephrine whereas clonidine, xylazine, B-HT 920 and B-HT 933 produced minimal contractions. Prazosin competitively inhibited the contractile response to phenylephrine (pA2 = 8.6), whereas rauwolscine caused a noncompetitive inhibition and was more than 100 times less potent than prazosin at inhibiting the response to phenylephrine. Similar results were obtained using norepinephrine (in the presence of propranolol) as the agonist. The calcium-entry blockers nimodipine, verapamil and diltiazem inhibited contractions caused by norepinephrine, phenylephrine and cirazoline. Removal of extracellular calcium abolished the response to cirazoline. These results suggest that in large canine coronary arteries: 1) only alpha-1 adrenoceptors are present postjunctionally and 2) responses due to alpha-1 adrenoceptor activation are dependent upon extracellular calcium.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.meshAdrenergic Alpha-Agonists - Pharmacologyen_US
dc.subject.meshAdrenergic Alpha-Antagonists - Pharmacologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshCalcium - Metabolismen_US
dc.subject.meshCalcium Channel Blockers - Pharmacologyen_US
dc.subject.meshClonidine - Pharmacologyen_US
dc.subject.meshCoronary Vessels - Drug Effectsen_US
dc.subject.meshDogsen_US
dc.subject.meshFemaleen_US
dc.subject.meshImidazoles - Pharmacologyen_US
dc.subject.meshMaleen_US
dc.subject.meshMethoxamine - Pharmacologyen_US
dc.subject.meshMuscle Contraction - Drug Effectsen_US
dc.subject.meshNorepinephrine - Pharmacologyen_US
dc.subject.meshPhenylephrine - Pharmacologyen_US
dc.subject.meshPrazosin - Pharmacologyen_US
dc.subject.meshSecologanin Tryptamine Alkaloidsen_US
dc.subject.meshYohimbine - Pharmacologyen_US
dc.titleAlpha-1 adrenoceptors and calcium in isolated canine coronary arteriesen_US
dc.typeArticleen_US
dc.identifier.emailVanhoutte, PM:vanhoutt@hku.hken_US
dc.identifier.authorityVanhoutte, PM=rp00238en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.pmid6136598-
dc.identifier.scopuseid_2-s2.0-0020516008en_US
dc.identifier.volume226en_US
dc.identifier.issue3en_US
dc.identifier.spage668en_US
dc.identifier.epage672en_US
dc.identifier.isiWOS:A1983RJ08500007-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridRimele, TJ=7004614618en_US
dc.identifier.scopusauthoridRooke, TW=8757981200en_US
dc.identifier.scopusauthoridAarhus, LL=7003305335en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

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