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Article: Differential sensitivity to endothelin in canine arteries and veins

TitleDifferential sensitivity to endothelin in canine arteries and veins
Authors
Issue Date1989
PublisherAmerican Physiological Society. The Journal's web site is located at http://ajpcon.physiology.org/
Citation
American Journal Of Physiology - Heart And Circulatory Physiology, 1989, v. 257 n. 4, p. 26/4 How to Cite?
AbstractExperiments were designed to compare the sensitivity of venous and arterial smooth muscle to endothelin and to determine whether contractions to the peptide could be inhibited by endothelium-derived relaxing factor and nitric oxide. Rings of canine left anterior descending coronary, femoral, and mesenteric arteries and femoral and saphenous veins with and without endothelium were suspended for measurement of isometric force. In the presence of indomethacin, phentolamine, and propranolol, endothelin initiated concentration-dependent increases in tension in all rings. The veins were more sensitive to the peptide than were the arteries. Endothelin depolarized the smooth muscle of the saphenous veins and mesenteric arteries; the threshold concentration for depolarization was ~ 100 times lower in the veins (10-10 M) than in the arteries (10-8 M). Removal of the endothelium enhanced the sensitivity only of venous smooth muscle to endothelin. However, stimulation of the endothelium in the arteries with either acetylcholine or the calcium ionophore A23187 rapidly inhibited the maximal tension developed to the peptide. Nitric oxide inhibited contractions to endothelin in arteries and veins without endothelium; the inhibition was greater in the arteries than in the veins. These results indicate that venous smooth muscle is more sensitive than arterial smooth muscle to endothelin. In both blood vessels, endothelium-derived relaxin factor(s) can inhibit contractions to the peptide.
Persistent Identifierhttp://hdl.handle.net/10722/170937
ISSN
1998 Impact Factor: 3.077
2004 SCImago Journal Rankings: 1.102

 

DC FieldValueLanguage
dc.contributor.authorMiller, VMen_US
dc.contributor.authorKomori, Ken_US
dc.contributor.authorBurnett Jr, JCen_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:11:30Z-
dc.date.available2012-10-30T06:11:30Z-
dc.date.issued1989en_US
dc.identifier.citationAmerican Journal Of Physiology - Heart And Circulatory Physiology, 1989, v. 257 n. 4, p. 26/4en_US
dc.identifier.issn0002-9513en_US
dc.identifier.urihttp://hdl.handle.net/10722/170937-
dc.description.abstractExperiments were designed to compare the sensitivity of venous and arterial smooth muscle to endothelin and to determine whether contractions to the peptide could be inhibited by endothelium-derived relaxing factor and nitric oxide. Rings of canine left anterior descending coronary, femoral, and mesenteric arteries and femoral and saphenous veins with and without endothelium were suspended for measurement of isometric force. In the presence of indomethacin, phentolamine, and propranolol, endothelin initiated concentration-dependent increases in tension in all rings. The veins were more sensitive to the peptide than were the arteries. Endothelin depolarized the smooth muscle of the saphenous veins and mesenteric arteries; the threshold concentration for depolarization was ~ 100 times lower in the veins (10-10 M) than in the arteries (10-8 M). Removal of the endothelium enhanced the sensitivity only of venous smooth muscle to endothelin. However, stimulation of the endothelium in the arteries with either acetylcholine or the calcium ionophore A23187 rapidly inhibited the maximal tension developed to the peptide. Nitric oxide inhibited contractions to endothelin in arteries and veins without endothelium; the inhibition was greater in the arteries than in the veins. These results indicate that venous smooth muscle is more sensitive than arterial smooth muscle to endothelin. In both blood vessels, endothelium-derived relaxin factor(s) can inhibit contractions to the peptide.en_US
dc.languageengen_US
dc.publisherAmerican Physiological Society. The Journal's web site is located at http://ajpcon.physiology.org/en_US
dc.relation.ispartofAmerican Journal of Physiology - Heart and Circulatory Physiologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshArteries - Drug Effects - Physiologyen_US
dc.subject.meshDogsen_US
dc.subject.meshEndothelinsen_US
dc.subject.meshEndothelium, Vascular - Physiologyen_US
dc.subject.meshKineticsen_US
dc.subject.meshMembrane Potentials - Drug Effectsen_US
dc.subject.meshMesenteric Arteries - Physiologyen_US
dc.subject.meshMicroelectrodesen_US
dc.subject.meshMuscle, Smooth, Vascular - Drug Effects - Physiologyen_US
dc.subject.meshPeptides - Pharmacologyen_US
dc.subject.meshSaphenous Vein - Physiologyen_US
dc.subject.meshVeins - Drug Effects - Physiologyen_US
dc.titleDifferential sensitivity to endothelin in canine arteries and veinsen_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.pmid2679147-
dc.identifier.scopuseid_2-s2.0-0024440075en_US
dc.identifier.volume257en_US
dc.identifier.issue4en_US
dc.identifier.spage26/4en_US
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridMiller, VM=7201476816en_US
dc.identifier.scopusauthoridKomori, K=8977740100en_US
dc.identifier.scopusauthoridBurnett Jr, JC=35391042200en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

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