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Article: Prostacyclin-induced relaxations of small porcine pulmonary arteries are enhanced by the basal release of endothelium-derived nitric oxide through an effect on cyclic GMP-inhibited-cyclic AMP phosphodiesterase

TitleProstacyclin-induced relaxations of small porcine pulmonary arteries are enhanced by the basal release of endothelium-derived nitric oxide through an effect on cyclic GMP-inhibited-cyclic AMP phosphodiesterase
Authors
Issue Date2000
Citation
Acta Pharmacologica Sinica, 2000, v. 21 n. 2, p. 131-138 How to Cite?
AbstractAIM: To study the interactions between prostacyclin and endothelium- derived nitric oxide in porcine pulmonary arteries. METHODS: Rings of 5th order of porcine pulmonary arteries were studied in vitro for the measurement of tension and the content in cyclic nucleotides. RESULTS: Prostacyclin, given exogenously, caused endothelium-potentiated relaxations (inhibition of phenylephrine contraction) that were inhibited by the inhibitors of the L- arginine nitric oxide pathway, oxyhemoglobin and N(ω)-nitro-L-arginine. These inhibitors did not affect the tension in rings without endothelium. Cyclic GMP-concentrations were not increased above basal concentrations in the presence of prostacyclin. Increases were seen with acetylcholine and sodium nitroprusside. Prostacyclin-stimulated cyclic AMP concentrations did not reach statistical significance compared to controls. The addition of 8- bromo-cyclic GMP to prostacyclin, however, increased the cyclic AMP content. The nitric oxide synthase inhibitor, nitro-L-arginine (NLA), reduced the prostacyclin-stimulated cyclic AMP content to basal level. Inhibition of cyclic GMP-inhibited cyclic AMP phosphodiesterase by 8-bromo-cyclic GMP or amrinone (a specific inhibitor of this enzyme) potentiated the prostacyclin- induced relaxations in rings without endothelium to a magnitude similar to that observed in rings with endothelium. CONCLUSION: These data suggest that the augmentation by the endothelium of the prostacyclin-induced relaxation of porcine pulmonary arteries is secondary to the inhibition of cyclic GMP- inhibited cyclic AMP phosphodiesterase by basally released endothelium- derived nitric oxide.
Persistent Identifierhttp://hdl.handle.net/10722/171247
ISSN
2000 Impact Factor: 0.485
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorZellers, TMen_US
dc.contributor.authorWu, YQen_US
dc.contributor.authorMccormick, Jen_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:12:56Z-
dc.date.available2012-10-30T06:12:56Z-
dc.date.issued2000en_US
dc.identifier.citationActa Pharmacologica Sinica, 2000, v. 21 n. 2, p. 131-138en_US
dc.identifier.issn0253-9756en_US
dc.identifier.urihttp://hdl.handle.net/10722/171247-
dc.description.abstractAIM: To study the interactions between prostacyclin and endothelium- derived nitric oxide in porcine pulmonary arteries. METHODS: Rings of 5th order of porcine pulmonary arteries were studied in vitro for the measurement of tension and the content in cyclic nucleotides. RESULTS: Prostacyclin, given exogenously, caused endothelium-potentiated relaxations (inhibition of phenylephrine contraction) that were inhibited by the inhibitors of the L- arginine nitric oxide pathway, oxyhemoglobin and N(ω)-nitro-L-arginine. These inhibitors did not affect the tension in rings without endothelium. Cyclic GMP-concentrations were not increased above basal concentrations in the presence of prostacyclin. Increases were seen with acetylcholine and sodium nitroprusside. Prostacyclin-stimulated cyclic AMP concentrations did not reach statistical significance compared to controls. The addition of 8- bromo-cyclic GMP to prostacyclin, however, increased the cyclic AMP content. The nitric oxide synthase inhibitor, nitro-L-arginine (NLA), reduced the prostacyclin-stimulated cyclic AMP content to basal level. Inhibition of cyclic GMP-inhibited cyclic AMP phosphodiesterase by 8-bromo-cyclic GMP or amrinone (a specific inhibitor of this enzyme) potentiated the prostacyclin- induced relaxations in rings without endothelium to a magnitude similar to that observed in rings with endothelium. CONCLUSION: These data suggest that the augmentation by the endothelium of the prostacyclin-induced relaxation of porcine pulmonary arteries is secondary to the inhibition of cyclic GMP- inhibited cyclic AMP phosphodiesterase by basally released endothelium- derived nitric oxide.en_US
dc.languageengen_US
dc.relation.ispartofActa Pharmacologica Sinicaen_US
dc.subject.mesh3',5'-Cyclic-Amp Phosphodiesterases - Metabolismen_US
dc.subject.meshAnimalsen_US
dc.subject.meshCyclic Amp - Metabolismen_US
dc.subject.meshCyclic Gmp - Analogs & Derivatives - Metabolism - Pharmacologyen_US
dc.subject.meshEndothelium, Vascular - Metabolismen_US
dc.subject.meshEpoprostenol - Pharmacologyen_US
dc.subject.meshNitric Oxide - Biosynthesis - Physiologyen_US
dc.subject.meshPulmonary Artery - Drug Effectsen_US
dc.subject.meshSwine, Miniatureen_US
dc.subject.meshVasodilation - Drug Effectsen_US
dc.titleProstacyclin-induced relaxations of small porcine pulmonary arteries are enhanced by the basal release of endothelium-derived nitric oxide through an effect on cyclic GMP-inhibited-cyclic AMP phosphodiesteraseen_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.pmid11263259-
dc.identifier.scopuseid_2-s2.0-0034141216en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0034141216&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume21en_US
dc.identifier.issue2en_US
dc.identifier.spage131en_US
dc.identifier.epage138en_US
dc.identifier.isiWOS:000085208200005-
dc.identifier.scopusauthoridZellers, TM=6701423788en_US
dc.identifier.scopusauthoridWu, YQ=7406899135en_US
dc.identifier.scopusauthoridMcCormick, J=23393010500en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

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