File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

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
KeywordsCyclic AMP
Cyclic GMP
Epoprostenol
Nitric acid
Phosphoric diester hydrolases
Pulmonary artery
Vascular endothelium
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.subjectCyclic AMP-
dc.subjectCyclic GMP-
dc.subjectEpoprostenol-
dc.subjectNitric acid-
dc.subjectPhosphoric diester hydrolases-
dc.subjectPulmonary artery-
dc.subjectVascular endothelium-
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
dc.identifier.issnl0253-9756-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats