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Conference Paper: Indapamide potentiates the endothelium-dependent production of cyclic guanosine monophosphate by bradykinin in the canine femoral artery

TitleIndapamide potentiates the endothelium-dependent production of cyclic guanosine monophosphate by bradykinin in the canine femoral artery
Authors
Issue Date1991
PublisherMosby, Inc. The Journal's web site is located at http://www.elsevier.com/locate/ahj
Citation
American Heart Journal, 1991, v. 122 n. 4 II, p. 1204-1209 How to Cite?
AbstractIndapamide is a sulfonamide diuretic agent that has antihypertensive properties. In the canine femoral artery, indomethacin reduces the endothelium-dependent relaxation induced by bradykinin, and indapamide restores the response. The aim of this study was to determine whether indapamide affects the release or the effects of endothelium-derived nitric oxide and prostanoids. The effect of indapamide on the production of endothelium-derived nitric oxide and prostacyclin was assessed indirectly by the measurement of the tissue content of cyclic guanosine monophosphate (GMP) and the accumulation of 6-keto-prostaglandin F(1α) in the incubation medium, respectively. Indapamide did not affect the basal production of either cyclic GMP, cyclic adenosine monophosphate (AMP), or 6-keto-prostaglandin F(1α) in the presence or absence of indomethacin. Indomethacin decreased the production of cyclic AMP and the release of 6-keto-prostaglandin F(1α) induced by bradykinin, and this was unaffected by indapamide. Indapamide enhanced the bradykinin-stimulated production of cyclic GMP in the presence of indomethacin and did not affect that evoked by 3 morpholino-sydnonimine, an exogenous donor of nitric oxide. Indomethacin had no significant effect on the production of cyclic GMP stimulated by either bradykinin or 3 morpholino-sydnonimine. These studies demonstrate that the potentiation by indapamide of the relaxation evoked by bradykinin is associated with an enhanced production of cyclic GMP in the presence of indomethacin, which suggests that the production of endothelium-derived nitric oxide is increased. This potentiation may be mediated by an interaction of indapamide with the prostacyclin and cyclic AMP pathways, or it may be associated with the scavening effect of indapamide against the oxygen-derived free radicals produced by the activation of arachidonic acid metabolism. Alternatively, an interaction of indapamide with the metabolism of kinins may contribute to the potentiation of the response to bradykinin.
Persistent Identifierhttp://hdl.handle.net/10722/173490
ISSN
2015 Impact Factor: 4.332
2015 SCImago Journal Rankings: 3.157
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorJunquero, DCen_US
dc.contributor.authorSchini, VBen_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:32:20Z-
dc.date.available2012-10-30T06:32:20Z-
dc.date.issued1991en_US
dc.identifier.citationAmerican Heart Journal, 1991, v. 122 n. 4 II, p. 1204-1209en_US
dc.identifier.issn0002-8703en_US
dc.identifier.urihttp://hdl.handle.net/10722/173490-
dc.description.abstractIndapamide is a sulfonamide diuretic agent that has antihypertensive properties. In the canine femoral artery, indomethacin reduces the endothelium-dependent relaxation induced by bradykinin, and indapamide restores the response. The aim of this study was to determine whether indapamide affects the release or the effects of endothelium-derived nitric oxide and prostanoids. The effect of indapamide on the production of endothelium-derived nitric oxide and prostacyclin was assessed indirectly by the measurement of the tissue content of cyclic guanosine monophosphate (GMP) and the accumulation of 6-keto-prostaglandin F(1α) in the incubation medium, respectively. Indapamide did not affect the basal production of either cyclic GMP, cyclic adenosine monophosphate (AMP), or 6-keto-prostaglandin F(1α) in the presence or absence of indomethacin. Indomethacin decreased the production of cyclic AMP and the release of 6-keto-prostaglandin F(1α) induced by bradykinin, and this was unaffected by indapamide. Indapamide enhanced the bradykinin-stimulated production of cyclic GMP in the presence of indomethacin and did not affect that evoked by 3 morpholino-sydnonimine, an exogenous donor of nitric oxide. Indomethacin had no significant effect on the production of cyclic GMP stimulated by either bradykinin or 3 morpholino-sydnonimine. These studies demonstrate that the potentiation by indapamide of the relaxation evoked by bradykinin is associated with an enhanced production of cyclic GMP in the presence of indomethacin, which suggests that the production of endothelium-derived nitric oxide is increased. This potentiation may be mediated by an interaction of indapamide with the prostacyclin and cyclic AMP pathways, or it may be associated with the scavening effect of indapamide against the oxygen-derived free radicals produced by the activation of arachidonic acid metabolism. Alternatively, an interaction of indapamide with the metabolism of kinins may contribute to the potentiation of the response to bradykinin.en_US
dc.languageengen_US
dc.publisherMosby, Inc. The Journal's web site is located at http://www.elsevier.com/locate/ahjen_US
dc.relation.ispartofAmerican Heart Journalen_US
dc.subject.meshAnimalsen_US
dc.subject.meshBradykinin - Pharmacologyen_US
dc.subject.meshCyclic Gmp - Biosynthesisen_US
dc.subject.meshDogsen_US
dc.subject.meshDrug Synergismen_US
dc.subject.meshEndothelium, Vascular - Drug Effects - Metabolismen_US
dc.subject.meshEpoprostenol - Secretionen_US
dc.subject.meshFemoral Artery - Drug Effects - Metabolismen_US
dc.subject.meshIndapamide - Pharmacologyen_US
dc.subject.meshIndomethacin - Pharmacologyen_US
dc.subject.meshMuscle, Smooth, Vascular - Drug Effectsen_US
dc.subject.meshNitric Oxide - Metabolismen_US
dc.titleIndapamide potentiates the endothelium-dependent production of cyclic guanosine monophosphate by bradykinin in the canine femoral arteryen_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.doi10.1016/0002-8703(91)90940-Jen_US
dc.identifier.pmid1656721-
dc.identifier.scopuseid_2-s2.0-0025914374en_US
dc.identifier.volume122en_US
dc.identifier.issue4 IIen_US
dc.identifier.spage1204en_US
dc.identifier.epage1209en_US
dc.identifier.isiWOS:A1991GJ61200003-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridJunquero, DC=26643025500en_US
dc.identifier.scopusauthoridSchini, VB=7004113565en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

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