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Article: Why are converting enzyme inhibitors vasodilators?

TitleWhy are converting enzyme inhibitors vasodilators?
Authors
Issue Date1989
PublisherBlackwell Publishing Ltd. The Journal's web site is located at http://www.blackwellpublishing.com/journals/BJCP
Citation
British Journal Of Clinical Pharmacology, 1989, v. 28 SUPPL. 2, p. 95S-104S How to Cite?
Abstract1. The primary action of the converting enzyme inhibitors to prevent the formation of angiotensin II can explain a decrease in peripheral vascular resistance in patients with elevated, but not in those with normal or reduced plasma renin levels. 2. The inhibition of the breakdown of bradykinin will potentiate the vasodilator properties of the endogenously produced peptide. These include direct relaxation of certain vascular smooth muscle, production of vasodilator prostanoids and release of endothelium-derived relaxing factor(s). The greater release of the latter in the kidney could exert a negative feedback on the release of renin. 3. In addition, converting enzyme inhibitors may directly (by a prejunctional effect) and indirectly (by curtailing the production of angiotensin II) reduce the release of noradrenaline in the blood vessel wall. 4. Converting enzyme inhibitors may also directly reduce the responsiveness of vascular smooth muscle to vasoconstrictor stimuli (e.g. α-adrenoceptor activation). 5. The different effects of these therapeutic agents may concur to induce peripheral vasodilatation.
Persistent Identifierhttp://hdl.handle.net/10722/170936
ISSN
2015 Impact Factor: 3.83
2015 SCImago Journal Rankings: 1.486
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorVanhoutte, PMen_US
dc.contributor.authorAuchSchwelk, Wen_US
dc.contributor.authorBiondi, MLen_US
dc.contributor.authorLorenz, RRen_US
dc.contributor.authorSchini, VBen_US
dc.contributor.authorVidal, MJen_US
dc.date.accessioned2012-10-30T06:11:30Z-
dc.date.available2012-10-30T06:11:30Z-
dc.date.issued1989en_US
dc.identifier.citationBritish Journal Of Clinical Pharmacology, 1989, v. 28 SUPPL. 2, p. 95S-104Sen_US
dc.identifier.issn0306-5251en_US
dc.identifier.urihttp://hdl.handle.net/10722/170936-
dc.description.abstract1. The primary action of the converting enzyme inhibitors to prevent the formation of angiotensin II can explain a decrease in peripheral vascular resistance in patients with elevated, but not in those with normal or reduced plasma renin levels. 2. The inhibition of the breakdown of bradykinin will potentiate the vasodilator properties of the endogenously produced peptide. These include direct relaxation of certain vascular smooth muscle, production of vasodilator prostanoids and release of endothelium-derived relaxing factor(s). The greater release of the latter in the kidney could exert a negative feedback on the release of renin. 3. In addition, converting enzyme inhibitors may directly (by a prejunctional effect) and indirectly (by curtailing the production of angiotensin II) reduce the release of noradrenaline in the blood vessel wall. 4. Converting enzyme inhibitors may also directly reduce the responsiveness of vascular smooth muscle to vasoconstrictor stimuli (e.g. α-adrenoceptor activation). 5. The different effects of these therapeutic agents may concur to induce peripheral vasodilatation.en_US
dc.languageengen_US
dc.publisherBlackwell Publishing Ltd. The Journal's web site is located at http://www.blackwellpublishing.com/journals/BJCPen_US
dc.relation.ispartofBritish Journal of Clinical Pharmacologyen_US
dc.subject.meshAngiotensin-Converting Enzyme Inhibitors - Pharmacologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshVasodilator Agents - Pharmacologyen_US
dc.titleWhy are converting enzyme inhibitors vasodilators?en_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.doi10.1111/j.1365-2125.1989.tb03585.x-
dc.identifier.pmid2690910-
dc.identifier.scopuseid_2-s2.0-0024437268en_US
dc.identifier.volume28en_US
dc.identifier.issueSUPPL. 2en_US
dc.identifier.spage95Sen_US
dc.identifier.epage104Sen_US
dc.identifier.isiWOS:A1989AZ39900002-
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US
dc.identifier.scopusauthoridAuchSchwelk, W=7003395589en_US
dc.identifier.scopusauthoridBiondi, ML=7005127265en_US
dc.identifier.scopusauthoridLorenz, RR=7402095192en_US
dc.identifier.scopusauthoridSchini, VB=7004113565en_US
dc.identifier.scopusauthoridVidal, MJ=7202764932en_US

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