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Article: Response to the endothelium-dependent vasodilator acetylcholine in perfused kidneys of normotensive and spontaneously hypertensive rats

TitleResponse to the endothelium-dependent vasodilator acetylcholine in perfused kidneys of normotensive and spontaneously hypertensive rats
Authors
Issue Date1993
PublisherInforma Healthcare. The Journal's web site is located at http://www.tandf.co.uk/journals/titles/08037051.html
Citation
Blood Pressure, 1993, v. 2 n. 3, p. 217-220 How to Cite?
AbstractThe possible role of endothelium-derived relaxing factor (EDRF) was investigated in resistance vessels of the kidney obtained from spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto (WKY) rats. Kidneys were studied in parallel and perfused with Tyrode's solution at constant optimal flow rates. In the presence of indomethacin, during vasoconstriction (increase in perfusion pressure) produced by prostaglandin F(2α), acetylcholine caused a graded dilatation (pressure fall) that was greater in kidneys of WKY than of SHR. Methylene blue and hydroquinone, but not oxyhemoglobin, inhibited the decreases in perfusion pressure induced by acetylcholine, but not those by papaverine. The results suggest that part of the renal vasodilatation induced by acetylcholine is mediated by endothelium-derived relaxing factor, and that the response is impaired in the resistance vessels of the hypertensive rat kidney.
Persistent Identifierhttp://hdl.handle.net/10722/171100
ISSN
2015 Impact Factor: 2.01
2015 SCImago Journal Rankings: 0.732

 

DC FieldValueLanguage
dc.contributor.authorTuncer, Men_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:12:11Z-
dc.date.available2012-10-30T06:12:11Z-
dc.date.issued1993en_US
dc.identifier.citationBlood Pressure, 1993, v. 2 n. 3, p. 217-220en_US
dc.identifier.issn0803-7051en_US
dc.identifier.urihttp://hdl.handle.net/10722/171100-
dc.description.abstractThe possible role of endothelium-derived relaxing factor (EDRF) was investigated in resistance vessels of the kidney obtained from spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto (WKY) rats. Kidneys were studied in parallel and perfused with Tyrode's solution at constant optimal flow rates. In the presence of indomethacin, during vasoconstriction (increase in perfusion pressure) produced by prostaglandin F(2α), acetylcholine caused a graded dilatation (pressure fall) that was greater in kidneys of WKY than of SHR. Methylene blue and hydroquinone, but not oxyhemoglobin, inhibited the decreases in perfusion pressure induced by acetylcholine, but not those by papaverine. The results suggest that part of the renal vasodilatation induced by acetylcholine is mediated by endothelium-derived relaxing factor, and that the response is impaired in the resistance vessels of the hypertensive rat kidney.en_US
dc.languageengen_US
dc.publisherInforma Healthcare. The Journal's web site is located at http://www.tandf.co.uk/journals/titles/08037051.htmlen_US
dc.relation.ispartofBlood Pressureen_US
dc.subject.meshAcetylcholine - Pharmacologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshHydroquinones - Pharmacologyen_US
dc.subject.meshHypertension - Physiopathologyen_US
dc.subject.meshIndomethacin - Pharmacologyen_US
dc.subject.meshKidney - Blood Supply - Drug Effects - Physiologyen_US
dc.subject.meshMethylene Blue - Pharmacologyen_US
dc.subject.meshNitric Oxide - Physiologyen_US
dc.subject.meshPerfusionen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Inbred Shren_US
dc.subject.meshRats, Inbred Wkyen_US
dc.subject.meshVascular Resistance - Drug Effects - Physiologyen_US
dc.subject.meshVasodilation - Drug Effects - Physiologyen_US
dc.titleResponse to the endothelium-dependent vasodilator acetylcholine in perfused kidneys of normotensive and spontaneously hypertensive ratsen_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.pmid8205316-
dc.identifier.scopuseid_2-s2.0-0027379863en_US
dc.identifier.volume2en_US
dc.identifier.issue3en_US
dc.identifier.spage217en_US
dc.identifier.epage220en_US
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridTuncer, M=55226796700en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

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