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Conference Paper: Relaxations to SIN-1, nitric oxide, and sodium nitroprusside in canine arteries and veins

TitleRelaxations to SIN-1, nitric oxide, and sodium nitroprusside in canine arteries and veins
Authors
KeywordsEndothelin
Endothelium
Molsidomine
Norepinephrine
Prostaglandin F<inf>2α</inf>
SIN-1
Vasodilation
Issue Date1989
PublisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.cardiovascularpharm.com/
Citation
Journal Of Cardiovascular Pharmacology, 1989, v. 14 SUPPL. 11, p. S67-S71 How to Cite?
AbstractExperiments were designed to compare the vasodilator properties of SIN-1, the active metabolite of molsidomine, with nitric oxide (NO) and sodium nitroprusside. Rings of canine femoral arteries and veins with and without endothelium were suspended in organ chambers for the measurement of isometric force. SIN-1 and sodium nitroprusside relaxed rings of blood vessels in the presence and in the absence of the endothelium. However, these relaxations were reduced by the endothelial cells in arteries contracted with endothelin and in veins contracted with prostaglandin F(2α). In the arteries, SIN-1, sodium nitroprusside, and NO were equipotent in relaxing rings without endothelium contracted with either norepinephrine or prostaglandin F(2α); NO was less potent than the other two vasodilators when the arteries were contracted with endothelin. In the veins without endothelium, the potency of the three nitrovasodilators was comparable; the veins were more sensitive to the effects of the dilators when contracted with prostaglandin F(2α) than with either endothelin or norepinephrine. These results indicate that SIN-1, sodium nitroprusside, and NO are potent dilators of arterial and venous smooth muscle, and that the potency of the dilators can be altered by endothelial cells and the contractile agonist differentially in arteries and veins.
Persistent Identifierhttp://hdl.handle.net/10722/173463
ISSN
2021 Impact Factor: 3.271
2020 SCImago Journal Rankings: 0.762
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorMiller, VMen_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:32:12Z-
dc.date.available2012-10-30T06:32:12Z-
dc.date.issued1989en_US
dc.identifier.citationJournal Of Cardiovascular Pharmacology, 1989, v. 14 SUPPL. 11, p. S67-S71en_US
dc.identifier.issn0160-2446en_US
dc.identifier.urihttp://hdl.handle.net/10722/173463-
dc.description.abstractExperiments were designed to compare the vasodilator properties of SIN-1, the active metabolite of molsidomine, with nitric oxide (NO) and sodium nitroprusside. Rings of canine femoral arteries and veins with and without endothelium were suspended in organ chambers for the measurement of isometric force. SIN-1 and sodium nitroprusside relaxed rings of blood vessels in the presence and in the absence of the endothelium. However, these relaxations were reduced by the endothelial cells in arteries contracted with endothelin and in veins contracted with prostaglandin F(2α). In the arteries, SIN-1, sodium nitroprusside, and NO were equipotent in relaxing rings without endothelium contracted with either norepinephrine or prostaglandin F(2α); NO was less potent than the other two vasodilators when the arteries were contracted with endothelin. In the veins without endothelium, the potency of the three nitrovasodilators was comparable; the veins were more sensitive to the effects of the dilators when contracted with prostaglandin F(2α) than with either endothelin or norepinephrine. These results indicate that SIN-1, sodium nitroprusside, and NO are potent dilators of arterial and venous smooth muscle, and that the potency of the dilators can be altered by endothelial cells and the contractile agonist differentially in arteries and veins.en_US
dc.languageengen_US
dc.publisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.cardiovascularpharm.com/en_US
dc.relation.ispartofJournal of Cardiovascular Pharmacologyen_US
dc.subjectEndothelin-
dc.subjectEndothelium-
dc.subjectMolsidomine-
dc.subjectNorepinephrine-
dc.subjectProstaglandin F<inf>2α</inf>-
dc.subjectSIN-1-
dc.subjectVasodilation-
dc.subject.meshAnalysis Of Varianceen_US
dc.subject.meshAnimalsen_US
dc.subject.meshDinoprost - Pharmacologyen_US
dc.subject.meshDogsen_US
dc.subject.meshEndothelins - Pharmacologyen_US
dc.subject.meshEndothelium, Vascularen_US
dc.subject.meshFemoral Artery - Drug Effectsen_US
dc.subject.meshFemoral Vein - Drug Effectsen_US
dc.subject.meshMolsidomine - Analogs & Derivatives - Pharmacologyen_US
dc.subject.meshMuscle Relaxation - Drug Effectsen_US
dc.subject.meshNitric Oxide - Pharmacologyen_US
dc.subject.meshNitroprusside - Pharmacologyen_US
dc.subject.meshNorepinephrine - Pharmacologyen_US
dc.subject.meshVasodilator Agents - Pharmacologyen_US
dc.titleRelaxations to SIN-1, nitric oxide, and sodium nitroprusside in canine arteries and veinsen_US
dc.typeConference_Paperen_US
dc.identifier.emailVanhoutte, PM:vanhoutt@hku.hken_US
dc.identifier.authorityVanhoutte, PM=rp00238en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1097/00005344-198914110-00012-
dc.identifier.pmid2484703-
dc.identifier.scopuseid_2-s2.0-0024823312en_US
dc.identifier.volume14en_US
dc.identifier.issueSUPPL. 11en_US
dc.identifier.spageS67en_US
dc.identifier.epageS71en_US
dc.identifier.isiWOS:A1989EC14200012-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridMiller, VM=7201476816en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US
dc.identifier.issnl0160-2446-

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