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Article: Pertussis toxin reduces endothelium-dependent and independent responses to alpha-2 adrenergic stimulation in systemic canine arteries and veins

TitlePertussis toxin reduces endothelium-dependent and independent responses to alpha-2 adrenergic stimulation in systemic canine arteries and veins
Authors
Issue Date1991
PublisherAmerican Society for Pharmacology and Experimental Therapeutics. The Journal's web site is located at http://jpet.aspetjournals.org
Citation
Journal Of Pharmacology And Experimental Therapeutics, 1991, v. 257 n. 1, p. 290-293 How to Cite?
AbstractA pertussis toxin-sensitive guanine nucleotide regulatory protein (G-protein) is involved in the signal transduction of certain endothelium-dependent responses in mammalian arteries. To determine whether a similar mechanism mediates endothelium-dependent responses in mammalian veins, rings of canine femoral arteries and veins with and without endothelium were suspended for the measurement of isometric force in organ chambers. In femoral arteries, incubation of the rings with pertussis toxin (from Bordetella pertussis, 100 ng/ml for 2 hr) in the presence of indomethacin and propranolol did not reduce significantly endothelium-dependent relaxations to acetylcholine and adenosine diphosphate, thrombin or the calcium ionophore A23187. However, endothelium-depondent relaxations evoked by the alpha-2 adrenergic agonist UK 14,304 were blocked by the pertussis toxin. In venous rings, endothelium-dependent relaxations to acetylcholine were reduced by the toxin, whereas the endothelium-dependent relaxations evoked by adenosine diphosphate, thrombin and A23187 were not affected. UK 14,304 contracted the veins; these contractions were augmented by removal of the endothelium. Pertussis toxin inhibited contractions to UK 14,304 in venous rings without but not with endothelium. Relaxations of arterial and venous smooth muscle to nitric oxide were unaffected by the toxin. Contractions to phenylephrine were not altered by either removal of the endothelium or the toxin in the arteries or veins. These results suggest that the release of endothelium-derived relaxing factor in response to stimulation of purine and thrombin receptors probably does not involve a pertussis toxin-sensitive G-protein in canine femoral arteries or veins. However, activation of such a protein may be necessary for the endothelial response to alpha-2 adrenergic stimulation in these blood vessels and for the contraction of venous smooth muscle evoked by alpha-2 adrenergic agonists.
Persistent Identifierhttp://hdl.handle.net/10722/171024
ISSN
2015 Impact Factor: 3.76
2015 SCImago Journal Rankings: 1.847
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorMiller, VMen_US
dc.contributor.authorFlavahan, NAen_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:11:52Z-
dc.date.available2012-10-30T06:11:52Z-
dc.date.issued1991en_US
dc.identifier.citationJournal Of Pharmacology And Experimental Therapeutics, 1991, v. 257 n. 1, p. 290-293en_US
dc.identifier.issn0022-3565en_US
dc.identifier.urihttp://hdl.handle.net/10722/171024-
dc.description.abstractA pertussis toxin-sensitive guanine nucleotide regulatory protein (G-protein) is involved in the signal transduction of certain endothelium-dependent responses in mammalian arteries. To determine whether a similar mechanism mediates endothelium-dependent responses in mammalian veins, rings of canine femoral arteries and veins with and without endothelium were suspended for the measurement of isometric force in organ chambers. In femoral arteries, incubation of the rings with pertussis toxin (from Bordetella pertussis, 100 ng/ml for 2 hr) in the presence of indomethacin and propranolol did not reduce significantly endothelium-dependent relaxations to acetylcholine and adenosine diphosphate, thrombin or the calcium ionophore A23187. However, endothelium-depondent relaxations evoked by the alpha-2 adrenergic agonist UK 14,304 were blocked by the pertussis toxin. In venous rings, endothelium-dependent relaxations to acetylcholine were reduced by the toxin, whereas the endothelium-dependent relaxations evoked by adenosine diphosphate, thrombin and A23187 were not affected. UK 14,304 contracted the veins; these contractions were augmented by removal of the endothelium. Pertussis toxin inhibited contractions to UK 14,304 in venous rings without but not with endothelium. Relaxations of arterial and venous smooth muscle to nitric oxide were unaffected by the toxin. Contractions to phenylephrine were not altered by either removal of the endothelium or the toxin in the arteries or veins. These results suggest that the release of endothelium-derived relaxing factor in response to stimulation of purine and thrombin receptors probably does not involve a pertussis toxin-sensitive G-protein in canine femoral arteries or veins. However, activation of such a protein may be necessary for the endothelial response to alpha-2 adrenergic stimulation in these blood vessels and for the contraction of venous smooth muscle evoked by alpha-2 adrenergic agonists.en_US
dc.languageengen_US
dc.publisherAmerican Society for Pharmacology and Experimental Therapeutics. The Journal's web site is located at http://jpet.aspetjournals.orgen_US
dc.relation.ispartofJournal of Pharmacology and Experimental Therapeuticsen_US
dc.subject.meshAnimalsen_US
dc.subject.meshDogsen_US
dc.subject.meshDose-Response Relationship, Drugen_US
dc.subject.meshEndothelium, Vascular - Physiologyen_US
dc.subject.meshFemoral Artery - Drug Effects - Physiologyen_US
dc.subject.meshFemoral Vein - Drug Effects - Physiologyen_US
dc.subject.meshPertussis Toxinen_US
dc.subject.meshQuinoxalines - Pharmacologyen_US
dc.subject.meshReceptors, Adrenergic, Alpha - Drug Effectsen_US
dc.subject.meshStimulation, Chemicalen_US
dc.subject.meshVasoconstriction - Drug Effectsen_US
dc.subject.meshVasodilation - Drug Effectsen_US
dc.subject.meshVirulence Factors, Bordetella - Pharmacologyen_US
dc.titlePertussis toxin reduces endothelium-dependent and independent responses to alpha-2 adrenergic stimulation in systemic canine arteries and veinsen_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.pmid1850467-
dc.identifier.scopuseid_2-s2.0-0026007020en_US
dc.identifier.volume257en_US
dc.identifier.issue1en_US
dc.identifier.spage290en_US
dc.identifier.epage293en_US
dc.identifier.isiWOS:A1991FH24000038-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridMiller, VM=7201476816en_US
dc.identifier.scopusauthoridFlavahan, NA=7006398882en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

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