Full metadata record

DC Field Value Language
dc.contributor.authorSeong Chun Kwon-
dc.contributor.authorWook Bum Pyun-
dc.contributor.authorGi Young Park-
dc.contributor.authorHee Kyung Choi-
dc.contributor.authorKwang Se Paik-
dc.contributor.authorBok Soon Kang-
dc.date.accessioned2018-08-21T16:30:37Z-
dc.date.available2018-08-21T16:30:37Z-
dc.date.issued1999-
dc.identifier.citationYonsei Medical Journal, Vol.40(4) : 331-338, 1999-
dc.identifier.issn0513-5796-
dc.identifier.otheroak-bbb-00035-
dc.identifier.urihttp://kumel.medlib.dsmc.or.kr/handle/2015.oak/37256-
dc.description.abstractExperiments were designed to characterize the cellular mechanisms of action of endothelium-derived vasodilator substances in the rabbit femoral artery. Acetylcholine (ACh, 10(-8)-10(-5) M) induced a concentration-dependent relaxation of isolated endothelium-intact arterial rings precontracted with norepinephrine (NE, 10(-6) M). The ACh-induced response was abolished by the removal of endothelium. NG-nitro-L-arginine (L-NAME, 10(-4) M), an inhibitor of NO synthase, partially inhibited ACh-induced endothelium-dependent relaxation, whereas indomethacin (10(-5) M) showed no effect on ACh-induced relaxation. 25 mM KCl partially inhibited ACh-induced relaxation by shifting the concentration-response curve and abolished the response when combined with L-NAME and NE. In the presence of L-NAME, ACh-induced relaxation was unaffected by glibenclamide (10(-5) M) but significantly reduced by apamin (10(-6) M), and almost completely blocked by tetraethylammonium (TEA, 10(-3) M), iberiotoxin (10(-7) M) and 4-aminopyridine (4-AP, 5 x 10(-3) M). The cytochrome P450 inhibitors, 7-ethoxyresorufin (7-ER, 10(-5) M) and miconazole (10(-5) M) also significantly inhibited ACh-induced relaxation. Ouabain (10(-6) M), an inhibitor of Na+, K(+)-ATPase, or K(+)-free solution, also significantly inhibited ACh-induced relaxation. ACh-induced relaxation was not significantly inhibited by 18-alpha-glycyrrhetinic acid (18 alpha-GA, 10(-4) M). These results of this study indicate that ACh-induced endothelium-dependent relaxation of the rabbit femoral artery occurs via a mechanism that involves activation of Na+, K(+)-ATPase and/or activation of both the voltage-gated K+ channel (Kv) and the large-conductance, Ca(2+)-activated K+ channel (BKCa). The results further suggest that EDHF released by ACh may be a cytochrome P450 product.-
dc.description.statementofresponsibilityopen-
dc.publisherSchool of Medicine-
dc.rightsBY_NC_ND-
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/2.0/kr-
dc.titleThe involvement of K+ channels and the possible pathway of EDHF in the rabbit femoral artery-
dc.typeArticle-
dc.contributor.localauthor박기영-
dc.contributor.alternativelocalauthorPark, Gi Young-
dc.contributor.departmentDept. of Rehabilitation Medicine (재활의학)-
dc.citation.volume40-
dc.citation.number4-
dc.citation.startpage331-
dc.citation.titleYonsei Medical Journal-
dc.citation.endpage338-
dc.identifier.doi10.3349/ymj.1999.40.4.331-


qrcode

Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.

BROWSE