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Conference Paper: Effects of indapamide on endothelium-dependent relaxations in isolated canine femoral arteries

TitleEffects of indapamide on endothelium-dependent relaxations in isolated canine femoral arteries
Authors
Issue Date1990
PublisherExcerpta Medica, Inc.. The Journal's web site is located at http://www.ajconline.org/
Citation
American Journal Of Cardiology, 1990, v. 65 n. 17, p. 6H-10H How to Cite?
AbstractIndapamide is an effecctive antihypertensive agent in humans and in experimental hypertensive animals. The aim of the present study was to investigate whether indapamide affects endothelium-dependent and independent relaxations in canine femoral arteries. Rings (with or without endothelium) were contracted with prostaglandin F(2α) (2 x 10-6 mol/liter) before the addition, in a cumulative fashion, of relaxing agents. Indapamide (10-7 to 10-4 mol/liter) had no direct effect on unstimulated or prostaglandin-stimulated preparations; it did not alter relaxations of preparations with endothelium induced by acetylcholine, bradykinin, adenosine diphosphate or the calcium ionophore A23187. Similarly, it did not affect relaxations induced by sodium nitroprusside, prostacyclin or forskolin in preparations with or without endothelium. Indomethacin shifted the concentration-response curve to bradykinin to the right and did not alter that to the other relaxing drugs. The reduced relaxation to bradykinin was reversed in a concentration-dependent manner by indapamide (10-7 to 10-5 mol/liter). In the presence of indomethacin, indapamide shifted the concentration response curve to prostacyclin (in rings with endothelium) and to forskolin (in rings with and without endothelium) to the left. Thus, indapamide does not directly affect endothelium-dependent and independent relaxations. However, when prostanoid production is impaired, indapamide facilitates the release of endothelium-derived relaxing factor(s), and to a lesser extent, the direct action on vascular smooth muscle of prostanoids (prostacyclin) released from the endothelium.
Persistent Identifierhttp://hdl.handle.net/10722/173478
ISSN
2015 Impact Factor: 3.154
2015 SCImago Journal Rankings: 2.063
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorSchini, VBen_US
dc.contributor.authorDewey, Jen_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:32:15Z-
dc.date.available2012-10-30T06:32:15Z-
dc.date.issued1990en_US
dc.identifier.citationAmerican Journal Of Cardiology, 1990, v. 65 n. 17, p. 6H-10Hen_US
dc.identifier.issn0002-9149en_US
dc.identifier.urihttp://hdl.handle.net/10722/173478-
dc.description.abstractIndapamide is an effecctive antihypertensive agent in humans and in experimental hypertensive animals. The aim of the present study was to investigate whether indapamide affects endothelium-dependent and independent relaxations in canine femoral arteries. Rings (with or without endothelium) were contracted with prostaglandin F(2α) (2 x 10-6 mol/liter) before the addition, in a cumulative fashion, of relaxing agents. Indapamide (10-7 to 10-4 mol/liter) had no direct effect on unstimulated or prostaglandin-stimulated preparations; it did not alter relaxations of preparations with endothelium induced by acetylcholine, bradykinin, adenosine diphosphate or the calcium ionophore A23187. Similarly, it did not affect relaxations induced by sodium nitroprusside, prostacyclin or forskolin in preparations with or without endothelium. Indomethacin shifted the concentration-response curve to bradykinin to the right and did not alter that to the other relaxing drugs. The reduced relaxation to bradykinin was reversed in a concentration-dependent manner by indapamide (10-7 to 10-5 mol/liter). In the presence of indomethacin, indapamide shifted the concentration response curve to prostacyclin (in rings with endothelium) and to forskolin (in rings with and without endothelium) to the left. Thus, indapamide does not directly affect endothelium-dependent and independent relaxations. However, when prostanoid production is impaired, indapamide facilitates the release of endothelium-derived relaxing factor(s), and to a lesser extent, the direct action on vascular smooth muscle of prostanoids (prostacyclin) released from the endothelium.en_US
dc.languageengen_US
dc.publisherExcerpta Medica, Inc.. The Journal's web site is located at http://www.ajconline.org/en_US
dc.relation.ispartofAmerican Journal of Cardiologyen_US
dc.subject.meshAcetylcholine - Pharmacologyen_US
dc.subject.meshAdenosine Diphosphate - Pharmacologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshBradykinin - Pharmacologyen_US
dc.subject.meshCalcimycin - Pharmacologyen_US
dc.subject.meshDinoprost - Pharmacologyen_US
dc.subject.meshDiuretics - Pharmacologyen_US
dc.subject.meshDogsen_US
dc.subject.meshDose-Response Relationship, Drugen_US
dc.subject.meshEndothelium, Vascular - Drug Effectsen_US
dc.subject.meshEpoprostenol - Pharmacologyen_US
dc.subject.meshFemaleen_US
dc.subject.meshFemoral Artery - Drug Effectsen_US
dc.subject.meshForskolin - Pharmacologyen_US
dc.subject.meshIndapamide - Pharmacologyen_US
dc.subject.meshIndomethacin - Pharmacologyen_US
dc.subject.meshMaleen_US
dc.subject.meshNitric Oxide - Pharmacokineticsen_US
dc.subject.meshVasodilation - Drug Effectsen_US
dc.titleEffects of indapamide on endothelium-dependent relaxations in isolated canine femoral arteriesen_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.doi10.1016/0002-9149(90)90336-Y-
dc.identifier.pmid2109928-
dc.identifier.scopuseid_2-s2.0-0025285813en_US
dc.identifier.volume65en_US
dc.identifier.issue17en_US
dc.identifier.spage6Hen_US
dc.identifier.epage10Hen_US
dc.identifier.isiWOS:A1990DB85900003-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridSchini, VB=7004113565en_US
dc.identifier.scopusauthoridDewey, J=36879630100en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

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