File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Rilmenidine activates postjunctianal alpha1- and alpha2-adrenoceptors in the canine saphenous vein

TitleRilmenidine activates postjunctianal alpha1- and alpha2-adrenoceptors in the canine saphenous vein
Authors
Issue Date1996
PublisherBlackwell Publishing Ltd. The Journal's web site is located at http://www.blackwellpublishing.com/journals/FCP
Citation
Fundamental And Clinical Pharmacology, 1996, v. 10 n. 4, p. 379-385 How to Cite?
AbstractExperiments were performed to determine the subtypes of alpha-adrenoceptors involved in the contraction induced by rilmenidine in isolated canine cutaneous veins. Rings of saphenous vein (without endothelium) were suspended for the recording of isometric force in physiological salt solution. All experiments were performed in the presence of propranolol (to antagonize beta-adrenoceptors), cocaine (to inhibit neuronal uptake) and hydrocortisone (to inhibit extraneuronal uptake). In the presence of rauwolscina (an alpha2-adrenegic blocker), rilmenidine caused concentration-dependent contractions which were inhibited by prazosin (nonselective alpha1-antagonist) and by (+)niguldipine (selective alpha(1A)-adrenergic antagonist), but not by (-)nigurdipine. After treatment with phenoxybenzamine (to alkylate alpha1-adrenoceptors), rilmenidine evoked contractions of the canine saphenous vein which were antagonized competitively by rauwolscine. The combination of rauwolscine and prazosin did not abolish contractions evoked by the highest concentrations of rilmenidine. Although binding experiments using 3H-idazoxan suggested the existence of a nonadrenergic binding site (around 20% of the total binding), contractile studies failed to demonstrate their involvement in the increases in tension evoked by rilmenidine. These experiments suggest that the contractions evoked by rilmenidine in isolated canine veins are mediated by both alpha(1A)- and alpha2-adrenoceptors.
Persistent Identifierhttp://hdl.handle.net/10722/171177
ISSN
2015 Impact Factor: 2.156
2015 SCImago Journal Rankings: 0.624
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorMarsault, Ren_US
dc.contributor.authorTaddei, Sen_US
dc.contributor.authorBoulanger, CMen_US
dc.contributor.authorIlliano, Sen_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:12:32Z-
dc.date.available2012-10-30T06:12:32Z-
dc.date.issued1996en_US
dc.identifier.citationFundamental And Clinical Pharmacology, 1996, v. 10 n. 4, p. 379-385en_US
dc.identifier.issn0767-3981en_US
dc.identifier.urihttp://hdl.handle.net/10722/171177-
dc.description.abstractExperiments were performed to determine the subtypes of alpha-adrenoceptors involved in the contraction induced by rilmenidine in isolated canine cutaneous veins. Rings of saphenous vein (without endothelium) were suspended for the recording of isometric force in physiological salt solution. All experiments were performed in the presence of propranolol (to antagonize beta-adrenoceptors), cocaine (to inhibit neuronal uptake) and hydrocortisone (to inhibit extraneuronal uptake). In the presence of rauwolscina (an alpha2-adrenegic blocker), rilmenidine caused concentration-dependent contractions which were inhibited by prazosin (nonselective alpha1-antagonist) and by (+)niguldipine (selective alpha(1A)-adrenergic antagonist), but not by (-)nigurdipine. After treatment with phenoxybenzamine (to alkylate alpha1-adrenoceptors), rilmenidine evoked contractions of the canine saphenous vein which were antagonized competitively by rauwolscine. The combination of rauwolscine and prazosin did not abolish contractions evoked by the highest concentrations of rilmenidine. Although binding experiments using 3H-idazoxan suggested the existence of a nonadrenergic binding site (around 20% of the total binding), contractile studies failed to demonstrate their involvement in the increases in tension evoked by rilmenidine. These experiments suggest that the contractions evoked by rilmenidine in isolated canine veins are mediated by both alpha(1A)- and alpha2-adrenoceptors.en_US
dc.languageengen_US
dc.publisherBlackwell Publishing Ltd. The Journal's web site is located at http://www.blackwellpublishing.com/journals/FCPen_US
dc.relation.ispartofFundamental and Clinical Pharmacologyen_US
dc.subject.meshAdrenergic Alpha-1 Receptor Agonistsen_US
dc.subject.meshAdrenergic Alpha-2 Receptor Agonistsen_US
dc.subject.meshAdrenergic Alpha-Agonists - Pharmacologyen_US
dc.subject.meshAdrenergic Alpha-Antagonists - Pharmacologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshCalcium Channel Blockers - Pharmacologyen_US
dc.subject.meshClonidine - Pharmacologyen_US
dc.subject.meshDihydropyridines - Pharmacologyen_US
dc.subject.meshDogsen_US
dc.subject.meshFemaleen_US
dc.subject.meshIdazoxan - Diagnostic Use - Metabolismen_US
dc.subject.meshImidazoles - Pharmacologyen_US
dc.subject.meshImidazoline Receptorsen_US
dc.subject.meshIsotope Labelingen_US
dc.subject.meshMaleen_US
dc.subject.meshMedetomidineen_US
dc.subject.meshMuscle Contraction - Drug Effectsen_US
dc.subject.meshMuscle, Smooth - Drug Effectsen_US
dc.subject.meshOsmolar Concentrationen_US
dc.subject.meshOxazoles - Pharmacologyen_US
dc.subject.meshPhenoxybenzamine - Pharmacologyen_US
dc.subject.meshPrazosin - Pharmacologyen_US
dc.subject.meshProtein Binding - Drug Effectsen_US
dc.subject.meshQuinoxalines - Pharmacologyen_US
dc.subject.meshRadioligand Assayen_US
dc.subject.meshReceptors, Adrenergic, Alpha-1 - Metabolismen_US
dc.subject.meshReceptors, Adrenergic, Alpha-2 - Metabolismen_US
dc.subject.meshReceptors, Drug - Drug Effectsen_US
dc.subject.meshSaphenous Vein - Drug Effects - Metabolismen_US
dc.subject.meshTritium - Diagnostic Useen_US
dc.subject.meshYohimbine - Pharmacologyen_US
dc.titleRilmenidine activates postjunctianal alpha1- and alpha2-adrenoceptors in the canine saphenous veinen_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.1472-8206.1996.tb00589.x-
dc.identifier.pmid8871137-
dc.identifier.scopuseid_2-s2.0-0029741335en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0029741335&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume10en_US
dc.identifier.issue4en_US
dc.identifier.spage379en_US
dc.identifier.epage385en_US
dc.identifier.isiWOS:A1996VB86900008-
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridMarsault, R=6603857574en_US
dc.identifier.scopusauthoridTaddei, S=7007037060en_US
dc.identifier.scopusauthoridBoulanger, CM=7006599024en_US
dc.identifier.scopusauthoridIlliano, S=6602119848en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats