Acute effects of 17β-estradiol on femoral veins from adult gonadally intact and ovariectomized female pigs

Our experiments were designed to determine the acute effects of 17β-estradiol on femoral veins from intact and ovariectomized female pigs. Rings of femoral veins with or without endothelium were suspended in organ chambers for measurement of isometric force. Concentration-response curves to 17β-estradiol (10^-9 to 10^-5 M) were obtained in veins contracted with prostaglandin F_aα in the absence and presence of inhibitors of either estrogen receptors (ICI-182780; 10^-5 M), nitric oxide synthase [N^G-monomethyl-L-arginine (L-NMMA); 10^-4 M], soluble guanylate cyclase (1-H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one; 10^-5 M), or potassium channels (tetraethylammonium; 10^-2 M). Estrogen receptors were identified with the use of Western blotting and immunostaining in veins of both groups. 17β-Estradiol caused acute endothelium-dependent relaxations in both groups. Relaxations to 17β-estradiol were inhibited by L-NMMA and 1-H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-l-one but not ICI-182780. Tetraethylammonium inhibited relaxations only in veins with endothelium from intact females. Results indicate that 17β-estradiol causes acute endothelium-dependent relaxations in femoral veins. The relative contribution of nitric oxide and K⁺ channels as mechanisms involved in relaxations to 17β-estradiol in femoral veins is modulated by ovarian status.