계명대학교 의학도서관 Repository

The involvement of K+ channels and the possible pathway of EDHF in the rabbit femoral artery

Metadata Downloads
Affiliated Author(s)
박기영
Alternative Author(s)
Park, Gi Young
Journal Title
Yonsei Medical Journal
ISSN
0513-5796
Issued Date
1999
Abstract
Experiments 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.
Department
Dept. of Rehabilitation Medicine (재활의학)
Publisher
School of Medicine
Citation
Seong Chun Kwon et al. (1999). The involvement of K+ channels and the possible pathway of EDHF in the rabbit femoral artery. Yonsei Medical Journal, 40(4), 331–338. doi: 10.3349/ymj.1999.40.4.331
Type
Article
ISSN
0513-5796
DOI
10.3349/ymj.1999.40.4.331
URI
https://kumel.medlib.dsmc.or.kr/handle/2015.oak/37256
Appears in Collections:
1. School of Medicine (의과대학) > Dept. of Rehabilitation Medicine (재활의학)
공개 및 라이선스
  • 공개 구분공개
파일 목록

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