Contribution of K+ channels to relaxation induced by 17 beta-estradiol but not by progesterone in isolated rat mesenteric artery rings
Publication in refereed journal

Times Cited
Web of Science22WOS source URL (as at 28/02/2021) Click here for the latest count
Altmetrics Information

Other information
Abstract17beta-Estradiol and progesterone were found to relax various vascular beds through multiple mechanisms. However, the exact ionic mechanisms underlying the acute relaxant responses to both hormones are incompletely understood. This study was aimed to examine the possible role of K+ channel activation in the relaxation induced by both hormones in isolated rat mesenteric artery rings. Isometric tension of each ring was measured with Grass force displacement transducers. In rat endothelium-denuded rings pre-constricted by 9,11-dideoxy-11alpha,9alpha-epoxy-methanoprostaglandin F-2alpha (U46619), the relaxation induced by 17beta-estradiol was partially inhibited by tetrapentylammonium, 4-aminopyridine, iberiotoxin, BaCl2, and tertiapin-Q but not by tetraethylammonium, charybdotoxin, apamin, or glibenclamide. In contrast, these putative K+ channel blockers, except for glibenclamide, did not affect the relaxant response to progesterone. In 4 x 10(-2) M K+-preconstricted rings, the K+ channel blockers lost their inhibitory effects on 17beta-estradiol-induced relaxation. Endothelium did not seem to be involved in the effects of K+ channel blockers on 17beta-estradiol-mediated relaxation. Nifedipine-induced relaxation was not inhibited but was instead enhanced by tetrapentylammonium, iberiotoxin, 4-aminopyridine, and BaCl2. The above results indicate that in rat mesenteric artery rings, nonselective activation of K+ channels contributes partially to the relaxation induced by 17beta-estradiol. These K+ channels involved in the estrogen response appeared to be sensitive to inhibition by K-Ca, K-V, and K-IR channel blockers. Lack of effect of K+ channel blockers on progesterone-induced relaxation suggests that these K+ channels play little or no role. The present findings provide pharmacological evidence for an additional mechanism contributing to acute vasorelaxation induced by 17beta-estradiol.
All Author(s) ListTsang SY, Yao XQ, Chan HY, Wong CM, Chen ZY, Au CL, Huang Y
Journal nameJournal of Cardiovascular Pharmacology
Volume Number41
Issue Number1
Pages4 - 13
LanguagesEnglish-United Kingdom
Keywords17 beta-estradiol; K+ channels; mesenteric artery; progesterone; rat; vasorelaxation
Web of Science Subject CategoriesCardiac & Cardiovascular Systems; CARDIAC & CARDIOVASCULAR SYSTEMS; Cardiovascular System & Cardiology; Pharmacology & Pharmacy; PHARMACOLOGY & PHARMACY

Last updated on 2021-01-03 at 01:20