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- Scopus: eid_2-s2.0-0034141216
- PMID: 11263259
- WOS: WOS:000085208200005
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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
Title | 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 |
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Authors | |
Keywords | Cyclic AMP Cyclic GMP Epoprostenol Nitric acid Phosphoric diester hydrolases Pulmonary artery Vascular endothelium |
Issue Date | 2000 |
Citation | Acta Pharmacologica Sinica, 2000, v. 21 n. 2, p. 131-138 How to Cite? |
Abstract | AIM: 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 Identifier | http://hdl.handle.net/10722/171247 |
ISSN | |
ISI Accession Number ID | |
References |
DC Field | Value | Language |
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dc.contributor.author | Zellers, TM | en_US |
dc.contributor.author | Wu, YQ | en_US |
dc.contributor.author | Mccormick, J | en_US |
dc.contributor.author | Vanhoutte, PM | en_US |
dc.date.accessioned | 2012-10-30T06:12:56Z | - |
dc.date.available | 2012-10-30T06:12:56Z | - |
dc.date.issued | 2000 | en_US |
dc.identifier.citation | Acta Pharmacologica Sinica, 2000, v. 21 n. 2, p. 131-138 | en_US |
dc.identifier.issn | 0253-9756 | en_US |
dc.identifier.uri | http://hdl.handle.net/10722/171247 | - |
dc.description.abstract | AIM: 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.language | eng | en_US |
dc.relation.ispartof | Acta Pharmacologica Sinica | en_US |
dc.subject | Cyclic AMP | - |
dc.subject | Cyclic GMP | - |
dc.subject | Epoprostenol | - |
dc.subject | Nitric acid | - |
dc.subject | Phosphoric diester hydrolases | - |
dc.subject | Pulmonary artery | - |
dc.subject | Vascular endothelium | - |
dc.subject.mesh | 3',5'-Cyclic-Amp Phosphodiesterases - Metabolism | en_US |
dc.subject.mesh | Animals | en_US |
dc.subject.mesh | Cyclic Amp - Metabolism | en_US |
dc.subject.mesh | Cyclic Gmp - Analogs & Derivatives - Metabolism - Pharmacology | en_US |
dc.subject.mesh | Endothelium, Vascular - Metabolism | en_US |
dc.subject.mesh | Epoprostenol - Pharmacology | en_US |
dc.subject.mesh | Nitric Oxide - Biosynthesis - Physiology | en_US |
dc.subject.mesh | Pulmonary Artery - Drug Effects | en_US |
dc.subject.mesh | Swine, Miniature | en_US |
dc.subject.mesh | Vasodilation - Drug Effects | en_US |
dc.title | 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 | en_US |
dc.type | Article | en_US |
dc.identifier.email | Vanhoutte, PM:vanhoutt@hku.hk | en_US |
dc.identifier.authority | Vanhoutte, PM=rp00238 | en_US |
dc.description.nature | link_to_subscribed_fulltext | en_US |
dc.identifier.pmid | 11263259 | - |
dc.identifier.scopus | eid_2-s2.0-0034141216 | en_US |
dc.relation.references | http://www.scopus.com/mlt/select.url?eid=2-s2.0-0034141216&selection=ref&src=s&origin=recordpage | en_US |
dc.identifier.volume | 21 | en_US |
dc.identifier.issue | 2 | en_US |
dc.identifier.spage | 131 | en_US |
dc.identifier.epage | 138 | en_US |
dc.identifier.isi | WOS:000085208200005 | - |
dc.identifier.scopusauthorid | Zellers, TM=6701423788 | en_US |
dc.identifier.scopusauthorid | Wu, YQ=7406899135 | en_US |
dc.identifier.scopusauthorid | McCormick, J=23393010500 | en_US |
dc.identifier.scopusauthorid | Vanhoutte, PM=7202304247 | en_US |
dc.identifier.issnl | 0253-9756 | - |