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Mechanism of L-NAME-resistant endothelium-dependent relaxation induced by acetylcholine in rabbit renal artery
DC Field | Value | Language |
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dc.contributor.author | 안덕선 | - |
dc.contributor.author | 이영호 | - |
dc.date.accessioned | 2019-11-11T05:19:55Z | - |
dc.date.available | 2019-11-11T05:19:55Z | - |
dc.date.issued | 2000 | - |
dc.identifier.issn | 1226-4512 | - |
dc.identifier.uri | https://ir.ymlib.yonsei.ac.kr/handle/22282913/171787 | - |
dc.description.abstract | In the rabbit renal artery, acetylcholine (ACh, 1 nM ~ 10 micrometer) induced endothelium-dependent relaxation of arterial rings precontracted with norepinephrine (NE, 1 micrometer) in a dose-dependent manner. NG-nitro-L-arginine (L-NAME, 0.1 mM), an inhibitor of NO synthase, or ODQ (1 micrometer), a soluble guanylate cyclase inhibitor, partially inhibited the ACh-induced endothelium-dependent relaxation. The ACh-induced relaxation was abolished in the presence of 25 mM KCl and L-NAME. The cytochrome P450 inhibitors, 7-ethoxyresorufin (7-ER, 10 micrometer), miconazole (10 micrometer), or 17-octadecynoic acid (17-ODYA, 10 micrometer), failed to inhibit the ACh-induced relaxation in the presence of L-NAME. 11,12-epoxyeicosatrienoic acid (11,12-EET, 10 micrometer) had no relaxant effect. The ACh-induced relaxation observed in the presence of L-NAME was significantly reduced by a combination of iberiotoxin (0.3 micrometer) and apamin (1 micrometer), and almost completely blocked by 4-aminopyridine (5 mM). The ACh-induced relaxation was antagonized by P2Y receptor antagonist, cibacron blue (10 and 100 micrometer), in a dose-dependent manner. Furthermore, 2-methylthio-ATP (2MeSATP), a potent P2Y agonist, induced the endothelium-dependent relaxation, and this relaxation was markedly reduced by either the combination of iberiotoxin and apamin or by cibacron blue. In conclusion, in renal arteries isolated from rabbit, ACh produced non-NO relaxation that is mediated by an EDHF. The results also suggest that ACh may activate the release of ATP from endothelial cells, which in turn activates P2Y receptor on the endothelial cells. Activation of endothelial P2Y receptors induces a release of EDHF resulting in a vasorelaxation via a mechanism that involves activation of both the voltage-gated K+ channels and the Ca2+-activated K+ channels. The results further suggest that EDHF does not appear to be a cytochrome P450 metabolite. | - |
dc.description.statementOfResponsibility | open | - |
dc.language | English | - |
dc.publisher | 대한약리학회 | - |
dc.relation.isPartOf | Korean Journal of Physiology & Pharmacology | - |
dc.rights | CC BY-NC-ND 2.0 KR | - |
dc.title | Mechanism of L-NAME-resistant endothelium-dependent relaxation induced by acetylcholine in rabbit renal artery | - |
dc.type | Article | - |
dc.contributor.college | College of Medicine (의과대학) | - |
dc.contributor.department | Dept. of Physiology (생리학교실) | - |
dc.contributor.googleauthor | Dong Soo Yeon | - |
dc.contributor.googleauthor | Duck Sun Ahn | - |
dc.contributor.googleauthor | Young-Ho Lee | - |
dc.contributor.googleauthor | Seong Chun Kwon | - |
dc.contributor.localId | A02223 | - |
dc.contributor.localId | A02968 | - |
dc.relation.journalcode | J02104 | - |
dc.identifier.eissn | 2093-3827 | - |
dc.subject.keyword | Acetylcholine | - |
dc.subject.keyword | Renal artery | - |
dc.subject.keyword | Endothelium-dependent relaxation | - |
dc.subject.keyword | EDHF | - |
dc.subject.keyword | K | - |
dc.subject.keyword | channel | - |
dc.subject.keyword | P2Y receptor | - |
dc.contributor.alternativeName | Ahn, Duk Sun | - |
dc.contributor.affiliatedAuthor | 안덕선 | - |
dc.contributor.affiliatedAuthor | 이영호 | - |
dc.citation.volume | 4 | - |
dc.citation.number | 6 | - |
dc.citation.startPage | 471 | - |
dc.citation.endPage | 477 | - |
dc.identifier.bibliographicCitation | Korean Journal of Physiology & Pharmacology, Vol.4(6) : 471-477, 2000 | - |
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