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Article: Inhibitors of prostaglandin synthesis augment β-adrenergic responsiveness in canine coronary arteries

TitleInhibitors of prostaglandin synthesis augment β-adrenergic responsiveness in canine coronary arteries
Authors
Issue Date1985
PublisherLippincott Williams & Wilkins. The Journal's web site is located at http://circres.ahajournals.org
Citation
Circulation Research, 1985, v. 56 n. 1, p. 117-125 How to Cite?
AbstractThe effects of inhibition of endogenous prostaglandin synthesis on the release of norepinephrine from sympathetic nerves and on postjunctional adrenergic responsiveness were studied in isolated canine left circumflex coronary arteries. In rings, suspended for isometric tension recording and contracted with prostaglandin F(2α), transmural electrical stimulation caused frequency-dependent relaxations, which were blocked by propranolol and augmented by indomethacin. In superfused strips, previously incubated with [3H]norepinephrine, electrical stimulation (2 Hz) increased the overflow of tritiated neurotransmitter; indomethacin did not influence basal or evoked [3H]norepinephrine overflow. Exogenous norepinephrine caused relaxations in rings contracted with prostaglandin F(2α), but increases in tension in potassium-depolarized tissues which could be abolished by phentolamine; isoproterenol induced relaxations in both cases. Indomethacin significantly augmented the relaxation in response to exogenous norepinephrine (during contractions with prostaglandin F(2α)) and reversed norepinephrine-induced contractions (during potassium-depolarization) into relaxation. Other cyclooxygenase inhibitors had comparable effects. In the presence of propranolol, indomethacin did not diminish contractions evoked by norepinephrine in depolarized rings. Relaxations induced by sodium nitroprusside or acetylcholine during contractions caused by prostaglandin F(2α) or potassium chloride were not affected by indomethacin. The augmentation of β-adrenergic responsiveness by indomethacin was abolished by exogenous prostacyclin. The prostacyclin synthetase inhibitor tranylcypromine and exogenous prostaglandin E2 depressed β-adrenergic responsiveness. Indomethacin did not affect the facilitatory action of phosphodiesterase inhibition on β-adrenergic relaxation. The data suggest that endogenous prostaglandins (most probably prostacyclin and prostaglandin E2) exert a 'braking' effect on β-adrenergic responsiveness in coronary arterial smooth muscle.
Persistent Identifierhttp://hdl.handle.net/10722/170778
ISSN
2015 Impact Factor: 11.551
2015 SCImago Journal Rankings: 5.755
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorRubanyi, Gen_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:10:48Z-
dc.date.available2012-10-30T06:10:48Z-
dc.date.issued1985en_US
dc.identifier.citationCirculation Research, 1985, v. 56 n. 1, p. 117-125en_US
dc.identifier.issn0009-7330en_US
dc.identifier.urihttp://hdl.handle.net/10722/170778-
dc.description.abstractThe effects of inhibition of endogenous prostaglandin synthesis on the release of norepinephrine from sympathetic nerves and on postjunctional adrenergic responsiveness were studied in isolated canine left circumflex coronary arteries. In rings, suspended for isometric tension recording and contracted with prostaglandin F(2α), transmural electrical stimulation caused frequency-dependent relaxations, which were blocked by propranolol and augmented by indomethacin. In superfused strips, previously incubated with [3H]norepinephrine, electrical stimulation (2 Hz) increased the overflow of tritiated neurotransmitter; indomethacin did not influence basal or evoked [3H]norepinephrine overflow. Exogenous norepinephrine caused relaxations in rings contracted with prostaglandin F(2α), but increases in tension in potassium-depolarized tissues which could be abolished by phentolamine; isoproterenol induced relaxations in both cases. Indomethacin significantly augmented the relaxation in response to exogenous norepinephrine (during contractions with prostaglandin F(2α)) and reversed norepinephrine-induced contractions (during potassium-depolarization) into relaxation. Other cyclooxygenase inhibitors had comparable effects. In the presence of propranolol, indomethacin did not diminish contractions evoked by norepinephrine in depolarized rings. Relaxations induced by sodium nitroprusside or acetylcholine during contractions caused by prostaglandin F(2α) or potassium chloride were not affected by indomethacin. The augmentation of β-adrenergic responsiveness by indomethacin was abolished by exogenous prostacyclin. The prostacyclin synthetase inhibitor tranylcypromine and exogenous prostaglandin E2 depressed β-adrenergic responsiveness. Indomethacin did not affect the facilitatory action of phosphodiesterase inhibition on β-adrenergic relaxation. The data suggest that endogenous prostaglandins (most probably prostacyclin and prostaglandin E2) exert a 'braking' effect on β-adrenergic responsiveness in coronary arterial smooth muscle.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.meshAcetylcholine - Pharmacologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshCoronary Vessels - Drug Effects - Innervationen_US
dc.subject.meshDinoprosten_US
dc.subject.meshDogsen_US
dc.subject.meshElectric Stimulationen_US
dc.subject.meshIndomethacin - Pharmacologyen_US
dc.subject.meshIsoproterenol - Pharmacologyen_US
dc.subject.meshMuscle Contractionen_US
dc.subject.meshMuscle, Smooth, Vascular - Drug Effects - Physiologyen_US
dc.subject.meshNitroprusside - Pharmacologyen_US
dc.subject.meshNorepinephrine - Metabolismen_US
dc.subject.meshPhentolamine - Pharmacologyen_US
dc.subject.meshPotassium Chloride - Pharmacologyen_US
dc.subject.meshPropranolol - Pharmacologyen_US
dc.subject.meshProstaglandin Antagonists - Pharmacologyen_US
dc.subject.meshProstaglandins F - Pharmacologyen_US
dc.subject.meshReceptors, Adrenergic, Beta - Drug Effects - Physiologyen_US
dc.subject.meshTranylcypromine - Pharmacologyen_US
dc.titleInhibitors of prostaglandin synthesis augment β-adrenergic responsiveness 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.pmid2981646-
dc.identifier.scopuseid_2-s2.0-0021958272en_US
dc.identifier.volume56en_US
dc.identifier.issue1en_US
dc.identifier.spage117en_US
dc.identifier.epage125en_US
dc.identifier.isiWOS:A1985AAV3500012-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridRubanyi, G=7005517991en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

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