Bracamonte, M. P., M. Jayachandran, K. S. Rud, and V. M. Miller. Acute effects of 17␤-estradiol on femoral veins from adult gonadally intact and ovariectomized female pigs. Our experiments were designed to determine the acute effects of 17␤-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 17␤-estradiol (10 Ϫ9 to 10 Ϫ5 M)

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... re obtained in veins contracted with prostaglandin F 2␣ in the absence and presence of inhibitors of either estrogen receptors (ICI-182780; 10 Ϫ5 M), nitric oxide synthase [N G -monomethyl-L-arginine (L-NMMA); 10 Ϫ4 M], soluble guanylate cyclase (1-H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one; 10 Ϫ5 M), or potassium channels (tetraethylammonium; 10 Ϫ2 M). Estrogen receptors were identified with the use of Western blotting and immunostaining in veins of both groups. 17␤-Estradiol caused acute endothelium-dependent relaxations in both groups. Relaxations to 17␤-estradiol were inhibited by L-NMMA and 1-H-[1,2,4]oxadiazolo[4,3a]quinoxalin-1-one but not ICI-182780. Tetraethylammonium inhibited relaxations only in veins with endothelium from intact females. Results indicate that 17␤-estradiol causes acute endothelium-dependent relaxations in femoral veins. The relative contribution of nitric oxide and K ϩ channels as mechanisms involved in relaxations to 17␤-estradiol in femoral veins is modulated by ovarian status. Address for reprint requests and other correspondence: V. M. Miller,