File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Conference Paper: The basal and stimulated release of EDRF inhibits the contractions evoked by endothelin-1 and endothelin-3 in aortae of normotensive and spontaneously hypertensive rats

TitleThe basal and stimulated release of EDRF inhibits the contractions evoked by endothelin-1 and endothelin-3 in aortae of normotensive and spontaneously hypertensive rats
Authors
Issue Date1991
PublisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.cardiovascularpharm.com/
Citation
Journal Of Cardiovascular Pharmacology, 1991, v. 17 SUPPL. 7, p. S267-S271 How to Cite?
AbstractEndothelin-1 (ET-1) evoked concentration-dependent contractions that were slow in onset and sustained in aortae from both normotensive (Wistar and Wistar-Kyoto rats) and spontaneously hypertensive rats. The presence of a functional endothelium reduced the contractions evoked by low concentrations of ET-1 in the aortae from normotensive rats and shifted the concentration-contraction curves to the right in the hypertensive rat. N(G)-monomethyl-L-arginine, a competitive inhibitor of nitric oxide (NO) synthase, inhibited the influence of the endothelium. Endothelin-3 (ET-3) evoked contractions in aortae from both normotensive and hypertensive rats at concentrations greater than 3 x 10-8 M, which were reduced by the presence of a functional endothelium. ET-1 and ET-3 evoked concentration- and endothelium-dependent relaxations in aortae contracted submaximally with phenylephrine, from both types of rats. The relaxations were reversed by methylene blue, an inhibitor of soluble guanylate cyclase, and nitro-L-arginine, a competitive inhibitor of NO synthase. These observations demonstrate that the endothelium modulates the contractile response evoked by ET-1 and ET-3 in the aorta of the rat. This inhibition is more pronounced in aortas from hypertensive compared to normotensive rats and is mediated, at least in part, by an enhanced production of endothelium-derived NO.
Persistent Identifierhttp://hdl.handle.net/10722/173497
ISSN
2015 Impact Factor: 2.462
2015 SCImago Journal Rankings: 0.962
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorSchini, VBen_US
dc.contributor.authorKim, NDen_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:32:21Z-
dc.date.available2012-10-30T06:32:21Z-
dc.date.issued1991en_US
dc.identifier.citationJournal Of Cardiovascular Pharmacology, 1991, v. 17 SUPPL. 7, p. S267-S271en_US
dc.identifier.issn0160-2446en_US
dc.identifier.urihttp://hdl.handle.net/10722/173497-
dc.description.abstractEndothelin-1 (ET-1) evoked concentration-dependent contractions that were slow in onset and sustained in aortae from both normotensive (Wistar and Wistar-Kyoto rats) and spontaneously hypertensive rats. The presence of a functional endothelium reduced the contractions evoked by low concentrations of ET-1 in the aortae from normotensive rats and shifted the concentration-contraction curves to the right in the hypertensive rat. N(G)-monomethyl-L-arginine, a competitive inhibitor of nitric oxide (NO) synthase, inhibited the influence of the endothelium. Endothelin-3 (ET-3) evoked contractions in aortae from both normotensive and hypertensive rats at concentrations greater than 3 x 10-8 M, which were reduced by the presence of a functional endothelium. ET-1 and ET-3 evoked concentration- and endothelium-dependent relaxations in aortae contracted submaximally with phenylephrine, from both types of rats. The relaxations were reversed by methylene blue, an inhibitor of soluble guanylate cyclase, and nitro-L-arginine, a competitive inhibitor of NO synthase. These observations demonstrate that the endothelium modulates the contractile response evoked by ET-1 and ET-3 in the aorta of the rat. This inhibition is more pronounced in aortas from hypertensive compared to normotensive rats and is mediated, at least in part, by an enhanced production of endothelium-derived NO.en_US
dc.languageengen_US
dc.publisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.cardiovascularpharm.com/en_US
dc.relation.ispartofJournal of Cardiovascular Pharmacologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshAorta, Thoracic - Drug Effects - Metabolism - Physiopathologyen_US
dc.subject.meshEndothelins - Pharmacologyen_US
dc.subject.meshHypertension - Physiopathologyen_US
dc.subject.meshMaleen_US
dc.subject.meshMuscle, Smooth, Vascular - Drug Effects - Physiology - Physiopathologyen_US
dc.subject.meshNitric Oxide - Metabolism - Physiologyen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Inbred Strainsen_US
dc.subject.meshRats, Inbred Wkyen_US
dc.subject.meshStimulation, Chemicalen_US
dc.subject.meshVasoconstriction - Drug Effectsen_US
dc.titleThe basal and stimulated release of EDRF inhibits the contractions evoked by endothelin-1 and endothelin-3 in aortae of normotensive and spontaneously hypertensive ratsen_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.doi10.1097/00005344-199100177-00076-
dc.identifier.pmid1725352-
dc.identifier.scopuseid_2-s2.0-0026322363en_US
dc.identifier.volume17en_US
dc.identifier.issueSUPPL. 7en_US
dc.identifier.spageS267en_US
dc.identifier.epageS271en_US
dc.identifier.isiWOS:A1991GU39600076-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridSchini, VB=7004113565en_US
dc.identifier.scopusauthoridKim, ND=7403396752en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats