Effect of 17β-estradiol exposure on vasorelaxation induced by K+ channel openers and Ca2+ channel blockers

17beta-Estradiol has been shown to relax blood vessels partly through inhibition of Ca2+ channels at supraphysiological concentrations; however, it is unknown whether acute exposure of the isolated artery rings to near physiological concentrations of sex steroid hormones could modulate the ionic channels that are involved in regulation of vascular tone. Brief incubation (20 min) with 17beta-estradiol (1-3 nmol/l) did not alter the relaxant response to three blocking agents of L-type voltage-sensitive Ca2+ channels, nifedipine, diltiazem and verapamil in either endothelium-intact or endothelium-denuded rat mesenteric artery rings. In contrast, 17beta-estradiol at 3 nmol/l significantly attenuated the relaxation induced by K+ channel openers, cromakalim and pinacidil in endothelium-denuded rings. Similarly, preincubation with progesterone (3 nmol/1) inhibited pinacidil-induced relaxation with much less effect on cromakalim-induced relaxation. It appears that 17beta-estradiol and progesterone attenuated the cromakalim- and pinacidil-induced relaxation in a different manner. These results suggest that acute exposure to female sex steroid hormones at near physiological levels may reduce the activity of ATP-sensitive K+ channels in the rat arteries. Copyright (C) 2002 S. Karger AG, Basel.