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Article: Dissociation between endothelium-dependent relaxations and increases in cGMP in systemic veins

TitleDissociation between endothelium-dependent relaxations and increases in cGMP in systemic veins
Authors
Issue Date1991
PublisherAmerican Physiological Society. The Journal's web site is located at http://ajpcon.physiology.org/
Citation
American Journal Of Physiology - Heart And Circulatory Physiology, 1991, v. 260 n. 5 29-5, p. H1531-H1537 How to Cite?
AbstractIn canine systemic veins, in contrast to what is observed in mammalian systemic arteries, endothelium-dependent relaxations to the calcium ionophore A23187 are not diminished by the inhibitor of soluble guanylate cyclase, methylene blue. Therefore, experiments were designed to determine whether these relaxations in the veins are associated with the accumulation of guanosine 3',5'-cyclic monophosphate (cGMP). Rings of canine femoral arteries and veins with and without endothelium were suspended for the measurement of isometric force in organ chambers; cGMP was measured by radioimmunoassay. In arteries and veins contracted with norepinephrine, the tissue content of cGMP was greater in rings with than without endothelium. This difference was decreased by methylene blue (10-5 M). A23187 (3 x 10-7 M, for 1 min) increased the accumulation of cGMP, which was temporally related with the onset of relaxation in tissues with endothelium. Methylene blue inhibited the accumulation of cGMP in both blood vessels but inhibited the relaxations only in the arteries. In rings without endothelium, sodium nitroprusside (3 x 10-7 and 10-5 M) initiated increases in cGMP, which followed the onset of relaxation. Neither response to sodium nitroprusside was reduced by methylene blue. These results suggest that in canine femoral arteries and veins, relaxation of the smooth muscle to sodium nitroprusside are mediated by a mechanism distinct from changes in cGMP. Likewise, in canine systemic veins, endothelium-derived factor(s) released in response to A23187 also can initiate relaxation of the smooth muscle by a mechanism distinct from changes in cGMP.
Persistent Identifierhttp://hdl.handle.net/10722/171011
ISSN
1998 Impact Factor: 3.077
2004 SCImago Journal Rankings: 1.102

 

DC FieldValueLanguage
dc.contributor.authorVidal, Men_US
dc.contributor.authorVanhoutte, PMen_US
dc.contributor.authorMiller, VMen_US
dc.date.accessioned2012-10-30T06:11:49Z-
dc.date.available2012-10-30T06:11:49Z-
dc.date.issued1991en_US
dc.identifier.citationAmerican Journal Of Physiology - Heart And Circulatory Physiology, 1991, v. 260 n. 5 29-5, p. H1531-H1537en_US
dc.identifier.issn0002-9513en_US
dc.identifier.urihttp://hdl.handle.net/10722/171011-
dc.description.abstractIn canine systemic veins, in contrast to what is observed in mammalian systemic arteries, endothelium-dependent relaxations to the calcium ionophore A23187 are not diminished by the inhibitor of soluble guanylate cyclase, methylene blue. Therefore, experiments were designed to determine whether these relaxations in the veins are associated with the accumulation of guanosine 3',5'-cyclic monophosphate (cGMP). Rings of canine femoral arteries and veins with and without endothelium were suspended for the measurement of isometric force in organ chambers; cGMP was measured by radioimmunoassay. In arteries and veins contracted with norepinephrine, the tissue content of cGMP was greater in rings with than without endothelium. This difference was decreased by methylene blue (10-5 M). A23187 (3 x 10-7 M, for 1 min) increased the accumulation of cGMP, which was temporally related with the onset of relaxation in tissues with endothelium. Methylene blue inhibited the accumulation of cGMP in both blood vessels but inhibited the relaxations only in the arteries. In rings without endothelium, sodium nitroprusside (3 x 10-7 and 10-5 M) initiated increases in cGMP, which followed the onset of relaxation. Neither response to sodium nitroprusside was reduced by methylene blue. These results suggest that in canine femoral arteries and veins, relaxation of the smooth muscle to sodium nitroprusside are mediated by a mechanism distinct from changes in cGMP. Likewise, in canine systemic veins, endothelium-derived factor(s) released in response to A23187 also can initiate relaxation of the smooth muscle by a mechanism distinct from changes in cGMP.en_US
dc.languageengen_US
dc.publisherAmerican Physiological Society. The Journal's web site is located at http://ajpcon.physiology.org/en_US
dc.relation.ispartofAmerican Journal of Physiology - Heart and Circulatory Physiologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshCalcimycin - Pharmacologyen_US
dc.subject.meshCyclic Gmp - Metabolismen_US
dc.subject.meshDogsen_US
dc.subject.meshEndothelium, Vascular - Physiologyen_US
dc.subject.meshFemaleen_US
dc.subject.meshFemoral Artery - Drug Effects - Metabolism - Physiologyen_US
dc.subject.meshFemoral Vein - Drug Effects - Metabolism - Physiologyen_US
dc.subject.meshMaleen_US
dc.subject.meshNitroprusside - Pharmacologyen_US
dc.subject.meshVasodilationen_US
dc.titleDissociation between endothelium-dependent relaxations and increases in cGMP in systemic 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.pmid1852123-
dc.identifier.scopuseid_2-s2.0-0025869982en_US
dc.identifier.volume260en_US
dc.identifier.issue5 29-5en_US
dc.identifier.spageH1531en_US
dc.identifier.epageH1537en_US
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridVidal, M=7202764932en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US
dc.identifier.scopusauthoridMiller, VM=7201476816en_US

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