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Article: Inhibition of the angiotensin converting enzyme by perindoprilat and release or nitric oxide

TitleInhibition of the angiotensin converting enzyme by perindoprilat and release or nitric oxide
Authors
Issue Date1995
PublisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/amjhyper
Citation
American Journal Of Hypertension, 1995, v. 8 n. 5 II SUPPL., p. 1S-6S How to Cite?
AbstractExperiments were designed to investigate the mechanism underlying the endothelium-dependent relaxations to perindoprilat, a converting enzyme inhibitor, in canine coronary arteries previously exposed to bradykinin. Rings suspended in organ chambers were exposed to bradykinin for 3 min and washed extensively for 150 min. In rings previously exposed to the peptide, bradykinin induced relaxations which were augmented in the presence of perindoprilat; this response was not affected by indomethacin, but nitro-L-arginine induced a rightward shift of the relaxation to the peptide without affecting its maximal effect. In canine coronary arteries previously exposed to the peptide, perindoprilat caused endothelium-dependent relaxations (IC50 = 7.83), which had been observed previously at concentrations where the converting enzyme inhibitor did not augment the response to bradykinin. Carboxypeptidase B2 but not aprotinin, impaired the relaxation to perindoprilat, suggesting a contribution of bradykinin. The relaxation to perindoprilat was not affected by the B2 antagonist Leu8-des-Arg9-bradykinin. However, the bradykinin B2 antagonist HOE-140 displayed a noncompetitive antagonism against the response to perindoprilat. The response to the converting enzyme inhibitor was not affected by indomethacin but was impaired significantly by nitro-L-arginine. The present findings suggest that in canine coronary arteries previously exposed to bradykinin, the relaxation to perindoprilat is mediated mainly by endothelium-derived nitric oxide. In addition, the response to perindoprilat may be due to factors other than just protection of bound bradykinin from degradation.
Persistent Identifierhttp://hdl.handle.net/10722/171165
ISSN
2015 Impact Factor: 3.182
2015 SCImago Journal Rankings: 1.397
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorDesta, Ben_US
dc.contributor.authorVanhoutte, PMen_US
dc.contributor.authorBoulanger, CMen_US
dc.date.accessioned2012-10-30T06:12:29Z-
dc.date.available2012-10-30T06:12:29Z-
dc.date.issued1995en_US
dc.identifier.citationAmerican Journal Of Hypertension, 1995, v. 8 n. 5 II SUPPL., p. 1S-6Sen_US
dc.identifier.issn0895-7061en_US
dc.identifier.urihttp://hdl.handle.net/10722/171165-
dc.description.abstractExperiments were designed to investigate the mechanism underlying the endothelium-dependent relaxations to perindoprilat, a converting enzyme inhibitor, in canine coronary arteries previously exposed to bradykinin. Rings suspended in organ chambers were exposed to bradykinin for 3 min and washed extensively for 150 min. In rings previously exposed to the peptide, bradykinin induced relaxations which were augmented in the presence of perindoprilat; this response was not affected by indomethacin, but nitro-L-arginine induced a rightward shift of the relaxation to the peptide without affecting its maximal effect. In canine coronary arteries previously exposed to the peptide, perindoprilat caused endothelium-dependent relaxations (IC50 = 7.83), which had been observed previously at concentrations where the converting enzyme inhibitor did not augment the response to bradykinin. Carboxypeptidase B2 but not aprotinin, impaired the relaxation to perindoprilat, suggesting a contribution of bradykinin. The relaxation to perindoprilat was not affected by the B2 antagonist Leu8-des-Arg9-bradykinin. However, the bradykinin B2 antagonist HOE-140 displayed a noncompetitive antagonism against the response to perindoprilat. The response to the converting enzyme inhibitor was not affected by indomethacin but was impaired significantly by nitro-L-arginine. The present findings suggest that in canine coronary arteries previously exposed to bradykinin, the relaxation to perindoprilat is mediated mainly by endothelium-derived nitric oxide. In addition, the response to perindoprilat may be due to factors other than just protection of bound bradykinin from degradation.en_US
dc.languageengen_US
dc.publisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/amjhyperen_US
dc.relation.ispartofAmerican Journal of Hypertensionen_US
dc.subject.meshAngiotensin-Converting Enzyme Inhibitors - Pharmacologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshAprotinin - Pharmacologyen_US
dc.subject.meshBradykinin - Antagonists & Inhibitors - Pharmacologyen_US
dc.subject.meshCarboxypeptidase Ben_US
dc.subject.meshCarboxypeptidases - Pharmacologyen_US
dc.subject.meshCoronary Vessels - Drug Effects - Metabolismen_US
dc.subject.meshDogsen_US
dc.subject.meshEndothelium, Vascular - Drug Effects - Metabolismen_US
dc.subject.meshFemaleen_US
dc.subject.meshIndoles - Pharmacologyen_US
dc.subject.meshMaleen_US
dc.subject.meshNitric Oxide - Metabolismen_US
dc.subject.meshVasodilation - Drug Effects - Physiologyen_US
dc.titleInhibition of the angiotensin converting enzyme by perindoprilat and release or nitric oxideen_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.doi10.1016/0895-7061(95)00026-L-
dc.identifier.pmid7544135-
dc.identifier.scopuseid_2-s2.0-0029033469en_US
dc.identifier.volume8en_US
dc.identifier.issue5 II SUPPL.en_US
dc.identifier.spage1Sen_US
dc.identifier.epage6Sen_US
dc.identifier.isiWOS:A1995RB67900001-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridDesta, B=6603788474en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US
dc.identifier.scopusauthoridBoulanger, CM=7006599024en_US

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