File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Chronic treatment with the Ca2+ channel inhibitor RO 40-5967 potentiates endothelium-dependent relaxations in the aorta of the hypertensive salt sensitive Dahl rat

TitleChronic treatment with the Ca2+ channel inhibitor RO 40-5967 potentiates endothelium-dependent relaxations in the aorta of the hypertensive salt sensitive Dahl rat
Authors
Issue Date1994
PublisherInforma Healthcare. The Journal's web site is located at http://www.tandf.co.uk/journals/titles/08037051.html
Citation
Blood Pressure, 1994, v. 3 n. 3, p. 193-196 How to Cite?
AbstractExperiments were designed to determine whether or not chronic treatment with the Ca2+ channel antagonist RO 40-5967 affects endothelium-dependent relaxations in the aorta of hypertensive, salt-sensitive Dahl rats. Salt- resistant and salt-sensitive Dahl rats were fed a diet containing 8% NaCl (for 8 weeks); in each group, half of the animals were given RO 40-5967 chronically (0.4 mg/l; in the drinking water). RO 40-5967 lowered arterial blood pressure in the salt-sensitive, hypertensive, but not in the salt- resistant, normotensive rats. Rings, with and without endothelium, of thoracic aortas were suspended for isometric tension recording in conventional organ chambers. The chronic treatment with RO 40-5967 potentiated endothelium-dependent relaxations to acetylcholine, adenosine- diphosphate and thrombin in preparations from salt-sensitive, but not in those of salt-resistant Dahl rats. The treatment also augmented, in aortas from salt-sensitive animals, the relaxations of rings without endothelium to the donor of nitric oxide, SIN-1. These experiments demonstrate that chronic administration of RO 40-5967 potentiates endothelium-dependent relaxations in arteries from animals with salt-induced hypertension. This potentiation can be explained in part by an augmented sensitivity of the vascular smooth muscle to endothelium-derived nitric oxide.
Persistent Identifierhttp://hdl.handle.net/10722/171136
ISSN
2015 Impact Factor: 2.01
2015 SCImago Journal Rankings: 0.732

 

DC FieldValueLanguage
dc.contributor.authorBoulanger, CMen_US
dc.contributor.authorDesta, Ben_US
dc.contributor.authorClozel, JPen_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:12:21Z-
dc.date.available2012-10-30T06:12:21Z-
dc.date.issued1994en_US
dc.identifier.citationBlood Pressure, 1994, v. 3 n. 3, p. 193-196en_US
dc.identifier.issn0803-7051en_US
dc.identifier.urihttp://hdl.handle.net/10722/171136-
dc.description.abstractExperiments were designed to determine whether or not chronic treatment with the Ca2+ channel antagonist RO 40-5967 affects endothelium-dependent relaxations in the aorta of hypertensive, salt-sensitive Dahl rats. Salt- resistant and salt-sensitive Dahl rats were fed a diet containing 8% NaCl (for 8 weeks); in each group, half of the animals were given RO 40-5967 chronically (0.4 mg/l; in the drinking water). RO 40-5967 lowered arterial blood pressure in the salt-sensitive, hypertensive, but not in the salt- resistant, normotensive rats. Rings, with and without endothelium, of thoracic aortas were suspended for isometric tension recording in conventional organ chambers. The chronic treatment with RO 40-5967 potentiated endothelium-dependent relaxations to acetylcholine, adenosine- diphosphate and thrombin in preparations from salt-sensitive, but not in those of salt-resistant Dahl rats. The treatment also augmented, in aortas from salt-sensitive animals, the relaxations of rings without endothelium to the donor of nitric oxide, SIN-1. These experiments demonstrate that chronic administration of RO 40-5967 potentiates endothelium-dependent relaxations in arteries from animals with salt-induced hypertension. This potentiation can be explained in part by an augmented sensitivity of the vascular smooth muscle to endothelium-derived nitric oxide.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.meshAnimalsen_US
dc.subject.meshAorta - Drug Effectsen_US
dc.subject.meshBenzimidazoles - Pharmacologyen_US
dc.subject.meshBlood Pressure - Drug Effectsen_US
dc.subject.meshCalcium Channel Blockers - Pharmacologyen_US
dc.subject.meshEndothelium, Vascular - Physiopathologyen_US
dc.subject.meshHypertension - Chemically Induced - Genetics - Physiopathologyen_US
dc.subject.meshMaleen_US
dc.subject.meshMibefradilen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Mutant Strainsen_US
dc.subject.meshReference Valuesen_US
dc.subject.meshSodium Chlorideen_US
dc.subject.meshTetrahydronaphthalenes - Pharmacologyen_US
dc.subject.meshTime Factorsen_US
dc.subject.meshVasodilation - Drug Effectsen_US
dc.subject.meshVasodilator Agents - Pharmacologyen_US
dc.titleChronic treatment with the Ca2+ channel inhibitor RO 40-5967 potentiates endothelium-dependent relaxations in the aorta of the hypertensive salt sensitive Dahl raten_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.pmid8069408-
dc.identifier.scopuseid_2-s2.0-0028183358en_US
dc.identifier.volume3en_US
dc.identifier.issue3en_US
dc.identifier.spage193en_US
dc.identifier.epage196en_US
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridBoulanger, CM=7006599024en_US
dc.identifier.scopusauthoridDesta, B=6603788474en_US
dc.identifier.scopusauthoridClozel, JP=7005974783en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats