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Article: Prejunctional and postjunctional actions of endogenous norepinephrine at the sympathetic neuroeffector junction in canine coronary arteries

TitlePrejunctional and postjunctional actions of endogenous norepinephrine at the sympathetic neuroeffector junction in canine coronary arteries
Authors
Issue Date1983
PublisherLippincott Williams & Wilkins. The Journal's web site is located at http://circres.ahajournals.org
Citation
Circulation Research, 1983, v. 52 n. 1, p. 16-25 How to Cite?
AbstractThe effects of endogenous and of exogenous norepinephrine were studied in isolated rings of canine left circumflex coronary artery and its first ventricular branch. Norepinephrine was released from adrenergic nerve endings by transmural electrical stimulation and by tyramine. In rings contracted with prostaglandin F(2α) transmural electrical stimulation resulted in frequency dependent relaxations which were blocked by propranolol or tetrodotoxin; tyramine and exogenous norepinephrine caused concentration-dependent relaxations which were blocked by propranolol. The tyramine-induced relaxations also were inhibited by cocaine. The left circumflex artery was less sensitive than its branch to β-adrenergic activation; this difference was significant even between rings of the two vessels immediately adjacent to the branching point and was abolished by phentolamine. In the presence of propranolol, transmural electrical stimulation, tyramine and phenylephrine, produced contractions of the left circumflex artery, but not the branch; these contractions were prevented by phentolamine. Phentolamine, but not prazosin, augmented the β-adrenergic response of left circumflex artery to low frequency stimulation; in arteries preincubated with 3H-norepinephrine, this was accompanied by an increased overflow to tritiated neurotransmitter. The prejunctional effect of phentolamine was also evident in branch coronary arteries which exhibit no postjunctional α-adrenergic responses. With high frequency stimulation, both α-adrenergic antagonists equally augmented the relaxation of left circumflex artery; the efflux of tritiated norepinephrine was not different from untreated arteries. These experiments demonstrate, in isolated coronary arteries, that the primary adrenergic response to released endogenous norephinephrine is β-adrenergic relaxation. The prejunctional effect of nonspecific α-adrenergic antagonists preclude their use in determining the importance of postjunctional coronary α-adrenergic receptor activation caused by sympathetic nerve stimulation.
Persistent Identifierhttp://hdl.handle.net/10722/170706
ISSN
2015 Impact Factor: 11.551
2015 SCImago Journal Rankings: 5.755
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorCohen, RAen_US
dc.contributor.authorShepherd, JTen_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:10:32Z-
dc.date.available2012-10-30T06:10:32Z-
dc.date.issued1983en_US
dc.identifier.citationCirculation Research, 1983, v. 52 n. 1, p. 16-25en_US
dc.identifier.issn0009-7330en_US
dc.identifier.urihttp://hdl.handle.net/10722/170706-
dc.description.abstractThe effects of endogenous and of exogenous norepinephrine were studied in isolated rings of canine left circumflex coronary artery and its first ventricular branch. Norepinephrine was released from adrenergic nerve endings by transmural electrical stimulation and by tyramine. In rings contracted with prostaglandin F(2α) transmural electrical stimulation resulted in frequency dependent relaxations which were blocked by propranolol or tetrodotoxin; tyramine and exogenous norepinephrine caused concentration-dependent relaxations which were blocked by propranolol. The tyramine-induced relaxations also were inhibited by cocaine. The left circumflex artery was less sensitive than its branch to β-adrenergic activation; this difference was significant even between rings of the two vessels immediately adjacent to the branching point and was abolished by phentolamine. In the presence of propranolol, transmural electrical stimulation, tyramine and phenylephrine, produced contractions of the left circumflex artery, but not the branch; these contractions were prevented by phentolamine. Phentolamine, but not prazosin, augmented the β-adrenergic response of left circumflex artery to low frequency stimulation; in arteries preincubated with 3H-norepinephrine, this was accompanied by an increased overflow to tritiated neurotransmitter. The prejunctional effect of phentolamine was also evident in branch coronary arteries which exhibit no postjunctional α-adrenergic responses. With high frequency stimulation, both α-adrenergic antagonists equally augmented the relaxation of left circumflex artery; the efflux of tritiated norepinephrine was not different from untreated arteries. These experiments demonstrate, in isolated coronary arteries, that the primary adrenergic response to released endogenous norephinephrine is β-adrenergic relaxation. The prejunctional effect of nonspecific α-adrenergic antagonists preclude their use in determining the importance of postjunctional coronary α-adrenergic receptor activation caused by sympathetic nerve stimulation.en_US
dc.languageengen_US
dc.publisherLippincott Williams & Wilkins. The Journal's web site is located at http://circres.ahajournals.orgen_US
dc.relation.ispartofCirculation Researchen_US
dc.subject.meshAdrenergic Alpha-Antagonists - Pharmacologyen_US
dc.subject.meshAngiotensin Ii - Pharmacologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshCocaine - Pharmacologyen_US
dc.subject.meshCoronary Vessels - Innervationen_US
dc.subject.meshDogsen_US
dc.subject.meshElectric Stimulationen_US
dc.subject.meshNeuroeffector Junction - Drug Effects - Physiologyen_US
dc.subject.meshNorepinephrine - Pharmacologyen_US
dc.subject.meshPhenylephrine - Pharmacologyen_US
dc.subject.meshPropranolol - Pharmacologyen_US
dc.subject.meshSympathetic Nervous System - Physiologyen_US
dc.subject.meshTyramine - Pharmacologyen_US
dc.subject.meshVasoconstriction - Drug Effectsen_US
dc.titlePrejunctional and postjunctional actions of endogenous norepinephrine at the sympathetic neuroeffector junction in 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.pmid6129074-
dc.identifier.scopuseid_2-s2.0-0020701457en_US
dc.identifier.volume52en_US
dc.identifier.issue1en_US
dc.identifier.spage16en_US
dc.identifier.epage25en_US
dc.identifier.isiWOS:A1983PZ88900003-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridCohen, RA=35562815800en_US
dc.identifier.scopusauthoridShepherd, JT=7401742522en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

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