File Download
There are no files associated with this item.
Links for fulltext
(May Require Subscription)
- Publisher Website: 10.1097/00005344-198914110-00016
- Scopus: eid_2-s2.0-0024828935
- PMID: 2484707
- WOS: WOS:A1989EC14200016
- Find via
Supplementary
- Citations:
- Appears in Collections:
Conference Paper: Mechanisms underlying the inhibitory interaction between the nitrovasodilator SIN-1 and the endothelium
Title | Mechanisms underlying the inhibitory interaction between the nitrovasodilator SIN-1 and the endothelium |
---|---|
Authors | |
Keywords | Catalase Coronary artery Endothelium L-NMMA Nitrovasodilator SIN-1 Superoxide dismutase |
Issue Date | 1989 |
Publisher | Lippincott Williams & Wilkins. The Journal's web site is located at http://www.cardiovascularpharm.com/ |
Citation | Journal Of Cardiovascular Pharmacology, 1989, v. 14 SUPPL. 11, p. S86-S90 How to Cite? |
Abstract | Experiments were designed to determine the influence of the endothelium on the relaxing potency of the nitrovasodilator SIN-1. Rings of coronary arteries were suspended for isometric-tension recording in organ chambers filled with modified Krebs-Ringer bicarbonate solution, aerated with 95% O2-5% CO2 and warmed to 37°C. The experiments were performed in the presence of indomethacin and propranolol in order to inhibit cyclooxygenase and β-adrenoceptors, respectively. In rings contracted with prostaglandin F(2α), SIN-1 caused concentration-dependent relaxations that were increased following endothelium removal. In rings denuded of endothelium, the relaxations evoked by SIN-1 were not affected by N(G)-monomethyl-L-arginine (L-NMMA, which inhibits the production of endothelium-derived relaxing factor), or by superoxide dismutase and catalase (scavengers of oxygen-derived free radicals), or by L-NMMA plus superoxide dismutase and catalase. In rings with endothelium, relaxations evoked by SIN-1 were increased significantly by L-NMMA or by superoxide dismutase and catalase, and were increased further by the combination of L-NMMA plus superoxide dismutase and catalase. The difference in potency of SIN-1 between arterial rings with and without endothelium was reduced by either L-NMMA or by superoxide dismutase and catalase, and was abolished by the combination of L-NMMA plus superoxide dismutase and catalase. Therefore, the inhibitory interaction between SIN-1 and the endothelium may result from an endothelium-dependent production of oxygen-derived free radicals that may inactivate the nitric oxide generated by SIN-1, and from an inhibitory interaction between SIN-1 and endothelium-derived relazxing factor, released under basal conditions. |
Persistent Identifier | http://hdl.handle.net/10722/173464 |
ISSN | 2023 Impact Factor: 2.6 2023 SCImago Journal Rankings: 0.610 |
ISI Accession Number ID |
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Flavahan, NA | en_US |
dc.contributor.author | Vanhoutte, PM | en_US |
dc.date.accessioned | 2012-10-30T06:32:12Z | - |
dc.date.available | 2012-10-30T06:32:12Z | - |
dc.date.issued | 1989 | en_US |
dc.identifier.citation | Journal Of Cardiovascular Pharmacology, 1989, v. 14 SUPPL. 11, p. S86-S90 | en_US |
dc.identifier.issn | 0160-2446 | en_US |
dc.identifier.uri | http://hdl.handle.net/10722/173464 | - |
dc.description.abstract | Experiments were designed to determine the influence of the endothelium on the relaxing potency of the nitrovasodilator SIN-1. Rings of coronary arteries were suspended for isometric-tension recording in organ chambers filled with modified Krebs-Ringer bicarbonate solution, aerated with 95% O2-5% CO2 and warmed to 37°C. The experiments were performed in the presence of indomethacin and propranolol in order to inhibit cyclooxygenase and β-adrenoceptors, respectively. In rings contracted with prostaglandin F(2α), SIN-1 caused concentration-dependent relaxations that were increased following endothelium removal. In rings denuded of endothelium, the relaxations evoked by SIN-1 were not affected by N(G)-monomethyl-L-arginine (L-NMMA, which inhibits the production of endothelium-derived relaxing factor), or by superoxide dismutase and catalase (scavengers of oxygen-derived free radicals), or by L-NMMA plus superoxide dismutase and catalase. In rings with endothelium, relaxations evoked by SIN-1 were increased significantly by L-NMMA or by superoxide dismutase and catalase, and were increased further by the combination of L-NMMA plus superoxide dismutase and catalase. The difference in potency of SIN-1 between arterial rings with and without endothelium was reduced by either L-NMMA or by superoxide dismutase and catalase, and was abolished by the combination of L-NMMA plus superoxide dismutase and catalase. Therefore, the inhibitory interaction between SIN-1 and the endothelium may result from an endothelium-dependent production of oxygen-derived free radicals that may inactivate the nitric oxide generated by SIN-1, and from an inhibitory interaction between SIN-1 and endothelium-derived relazxing factor, released under basal conditions. | en_US |
dc.language | eng | en_US |
dc.publisher | Lippincott Williams & Wilkins. The Journal's web site is located at http://www.cardiovascularpharm.com/ | en_US |
dc.relation.ispartof | Journal of Cardiovascular Pharmacology | en_US |
dc.subject | Catalase | - |
dc.subject | Coronary artery | - |
dc.subject | Endothelium | - |
dc.subject | L-NMMA | - |
dc.subject | Nitrovasodilator | - |
dc.subject | SIN-1 | - |
dc.subject | Superoxide dismutase | - |
dc.subject.mesh | Analysis Of Variance | en_US |
dc.subject.mesh | Animals | en_US |
dc.subject.mesh | Coronary Vessels - Drug Effects | en_US |
dc.subject.mesh | Dogs | en_US |
dc.subject.mesh | Female | en_US |
dc.subject.mesh | Free Radicals | en_US |
dc.subject.mesh | Male | en_US |
dc.subject.mesh | Molsidomine - Analogs & Derivatives - Pharmacology | en_US |
dc.subject.mesh | Nitric Oxide - Metabolism | en_US |
dc.subject.mesh | Vasodilator Agents - Pharmacology | en_US |
dc.title | Mechanisms underlying the inhibitory interaction between the nitrovasodilator SIN-1 and the endothelium | en_US |
dc.type | Conference_Paper | 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.doi | 10.1097/00005344-198914110-00016 | - |
dc.identifier.pmid | 2484707 | - |
dc.identifier.scopus | eid_2-s2.0-0024828935 | en_US |
dc.identifier.volume | 14 | en_US |
dc.identifier.issue | SUPPL. 11 | en_US |
dc.identifier.spage | S86 | en_US |
dc.identifier.epage | S90 | en_US |
dc.identifier.isi | WOS:A1989EC14200016 | - |
dc.publisher.place | United States | en_US |
dc.identifier.scopusauthorid | Flavahan, NA=7006398882 | en_US |
dc.identifier.scopusauthorid | Vanhoutte, PM=7202304247 | en_US |
dc.identifier.issnl | 0160-2446 | - |