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Article: Aggregating platelets contract isolated canine pulmonary arteries by releasing 5-hydroxytryptamine

TitleAggregating platelets contract isolated canine pulmonary arteries by releasing 5-hydroxytryptamine
Authors
Issue Date1984
PublisherAmerican Society for Clinical Investigation. The Journal's web site is located at http://www.jci.org
Citation
Journal Of Clinical Investigation, 1984, v. 74 n. 3, p. 828-833 How to Cite?
AbstractTo examine the effect of platelets and 5-hydroxytryptamine on pulmonary arterial smooth muscle, rings of canine pulmonary arteries, with and without endothelium, were studied under isometric conditions in physiological salt solution. 5-Hydroxytryptamine, but not the thromboxane-like endoperoxide analogue U-46619, produced concentration-dependent contractions of the rings with a maximum averaging 93% of that obtained with KCl. Autologous platelets in concentrations comparable to that in plasma caused contractions averaging 70% of the maximal responses to KCl. Solution withdrawn from baths containing platelet-contracted rings, but not the supernatant from nonaggregated platelets, also caused contraction. The serotonergic antagonists cyproheptadine, ketanserin, and methysergide caused concentration-dependent inhibition and eventually abolition of contractions evoked by platelets and 5-hydroxytryptamine. Phentolamine and prazosin produced significantly less inhibition of the contractile response to platelets. Pretreatment of the platelets with indomethacin or meclofenamate reduced thromboxane release but had no effect on platelet-induced contractions. Removal of the endothelium did not affect contractile responses to platelets or 5-hydroxytryptamine. These experiments demonstrate that in the canine pulmonary artery: (a) 5-hydroxytryptamine is the predominant mediator of the contractile response triggered by platelet aggregation; and (b) unlike in other blood vessels, the endothelium cannot curtail the contractile response to aggregating platelets.
Persistent Identifierhttp://hdl.handle.net/10722/170729
ISSN
2015 Impact Factor: 12.575
2015 SCImago Journal Rankings: 8.764
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorMcgoon, MDen_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:10:37Z-
dc.date.available2012-10-30T06:10:37Z-
dc.date.issued1984en_US
dc.identifier.citationJournal Of Clinical Investigation, 1984, v. 74 n. 3, p. 828-833en_US
dc.identifier.issn0021-9738en_US
dc.identifier.urihttp://hdl.handle.net/10722/170729-
dc.description.abstractTo examine the effect of platelets and 5-hydroxytryptamine on pulmonary arterial smooth muscle, rings of canine pulmonary arteries, with and without endothelium, were studied under isometric conditions in physiological salt solution. 5-Hydroxytryptamine, but not the thromboxane-like endoperoxide analogue U-46619, produced concentration-dependent contractions of the rings with a maximum averaging 93% of that obtained with KCl. Autologous platelets in concentrations comparable to that in plasma caused contractions averaging 70% of the maximal responses to KCl. Solution withdrawn from baths containing platelet-contracted rings, but not the supernatant from nonaggregated platelets, also caused contraction. The serotonergic antagonists cyproheptadine, ketanserin, and methysergide caused concentration-dependent inhibition and eventually abolition of contractions evoked by platelets and 5-hydroxytryptamine. Phentolamine and prazosin produced significantly less inhibition of the contractile response to platelets. Pretreatment of the platelets with indomethacin or meclofenamate reduced thromboxane release but had no effect on platelet-induced contractions. Removal of the endothelium did not affect contractile responses to platelets or 5-hydroxytryptamine. These experiments demonstrate that in the canine pulmonary artery: (a) 5-hydroxytryptamine is the predominant mediator of the contractile response triggered by platelet aggregation; and (b) unlike in other blood vessels, the endothelium cannot curtail the contractile response to aggregating platelets.en_US
dc.languageengen_US
dc.publisherAmerican Society for Clinical Investigation. The Journal's web site is located at http://www.jci.orgen_US
dc.relation.ispartofJournal of Clinical Investigationen_US
dc.subject.meshAnimalsen_US
dc.subject.meshBlood Platelets - Physiologyen_US
dc.subject.meshDogsen_US
dc.subject.meshEpinephrine - Metabolismen_US
dc.subject.meshKetanserinen_US
dc.subject.meshMuscle Contractionen_US
dc.subject.meshNorepinephrine - Metabolismen_US
dc.subject.meshPiperidines - Pharmacologyen_US
dc.subject.meshPlatelet Aggregationen_US
dc.subject.meshPulmonary Artery - Drug Effects - Physiologyen_US
dc.subject.meshSerotonin - Blood - Metabolism - Secretionen_US
dc.subject.meshSerotonin Antagonists - Pharmacologyen_US
dc.subject.meshThromboxane B2 - Blooden_US
dc.titleAggregating platelets contract isolated canine pulmonary arteries by releasing 5-hydroxytryptamineen_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.doi10.1172/JCI111499-
dc.identifier.pmid6470141-
dc.identifier.scopuseid_2-s2.0-0021174628en_US
dc.identifier.volume74en_US
dc.identifier.issue3en_US
dc.identifier.spage828en_US
dc.identifier.epage833en_US
dc.identifier.isiWOS:A1984TJ05800018-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridMcGoon, MD=7004310801en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

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