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Article: Vasoconstriction induced by ouabain in the canine coronary artery: contribution of adrenergic and nonadrenergic responses

TitleVasoconstriction induced by ouabain in the canine coronary artery: contribution of adrenergic and nonadrenergic responses
Authors
Issue Date1988
PublisherSpringer New York LLC. The Journal's web site is located at http://springerlink.metapress.com/openurl.asp?genre=journal&issn=0920-3206
Citation
Cardiovascular Drugs And Therapy, 1988, v. 2 n. 2, p. 255-263 How to Cite?
AbstractOuabain, when applied to rings of the left circumflex coronary artery of the dog (which contains both alpha1-adrenoceptors leading to contraction and beta1-adrenoceptors leading to relaxation) caused an initial contraction which peaked within 15 minutes and a later secondary increase in tension which peaked within 60 minutes. These contractions were prevented by Ca2+ removal or by verapamil. Adrenergic denervation with 6-hydroxydopamine did not affect the initial contraction. Thus it is due to a nonadrenergic effect of the glycoside. Since the secondary increase in tension was prevented by adrenergic denervation and prazosin, it is likely to be due to norepinephrine released from adrenergic nerves acting on alpha-adrenoceptors. This interpretation was confirmed by the finding that ouabain, after a latent period of about 35 minutes, augmented the output of 3H-norepinephrine from helical strips of the artery previously incubated with tritiated transmitter. In rings contracted with prostaglandin F(2α), ouabain reduced beta-adrenergic relaxations caused by isoproterenol or exogenous norepinephrine, but not those caused by sodium nitroprusside. Thus, in this artery, ouabain depresses the response of the beta-adrenoceptors to the norepinephrine which it releases, thereby permitting the neurotransmitter to cause contraction by activating postjunctional alpha1-adrenoceptors.
Persistent Identifierhttp://hdl.handle.net/10722/170869
ISSN
2015 Impact Factor: 3.189
2015 SCImago Journal Rankings: 1.114

 

DC FieldValueLanguage
dc.contributor.authorCooke, JPen_US
dc.contributor.authorShepherd, JTen_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:11:11Z-
dc.date.available2012-10-30T06:11:11Z-
dc.date.issued1988en_US
dc.identifier.citationCardiovascular Drugs And Therapy, 1988, v. 2 n. 2, p. 255-263en_US
dc.identifier.issn0920-3206en_US
dc.identifier.urihttp://hdl.handle.net/10722/170869-
dc.description.abstractOuabain, when applied to rings of the left circumflex coronary artery of the dog (which contains both alpha1-adrenoceptors leading to contraction and beta1-adrenoceptors leading to relaxation) caused an initial contraction which peaked within 15 minutes and a later secondary increase in tension which peaked within 60 minutes. These contractions were prevented by Ca2+ removal or by verapamil. Adrenergic denervation with 6-hydroxydopamine did not affect the initial contraction. Thus it is due to a nonadrenergic effect of the glycoside. Since the secondary increase in tension was prevented by adrenergic denervation and prazosin, it is likely to be due to norepinephrine released from adrenergic nerves acting on alpha-adrenoceptors. This interpretation was confirmed by the finding that ouabain, after a latent period of about 35 minutes, augmented the output of 3H-norepinephrine from helical strips of the artery previously incubated with tritiated transmitter. In rings contracted with prostaglandin F(2α), ouabain reduced beta-adrenergic relaxations caused by isoproterenol or exogenous norepinephrine, but not those caused by sodium nitroprusside. Thus, in this artery, ouabain depresses the response of the beta-adrenoceptors to the norepinephrine which it releases, thereby permitting the neurotransmitter to cause contraction by activating postjunctional alpha1-adrenoceptors.en_US
dc.languageengen_US
dc.publisherSpringer New York LLC. The Journal's web site is located at http://springerlink.metapress.com/openurl.asp?genre=journal&issn=0920-3206en_US
dc.relation.ispartofCardiovascular Drugs and Therapyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshCoronary Vessels - Drug Effectsen_US
dc.subject.meshDogsen_US
dc.subject.meshEpinephrine - Physiologyen_US
dc.subject.meshNorepinephrine - Physiologyen_US
dc.subject.meshOuabain - Pharmacologyen_US
dc.subject.meshSympathetic Nervous System - Drug Effects - Physiologyen_US
dc.subject.meshVasoconstriction - Drug Effectsen_US
dc.titleVasoconstriction induced by ouabain in the canine coronary artery: contribution of adrenergic and nonadrenergic responsesen_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.pmid3154710-
dc.identifier.scopuseid_2-s2.0-0023707429en_US
dc.identifier.volume2en_US
dc.identifier.issue2en_US
dc.identifier.spage255en_US
dc.identifier.epage263en_US
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridCooke, JP=7202378672en_US
dc.identifier.scopusauthoridShepherd, JT=7401742522en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

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