title: Acute effects of 17beta -estradiol on femoral veins from adult gonadally intact and ovariectomized female pigs.
abstract: Our experiments were designed to determine the acute effects of 17beta-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 17beta-estradiol (10(-9) to 10(-5) M) were obtained in veins contracted with prostaglandin F(2alpha) 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. 17beta-Estradiol caused acute endothelium-dependent relaxations in both groups. Relaxations to 17beta-estradiol were inhibited by l-NMMA and 1-H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one but not ICI-182780. Tetraethylammonium inhibited relaxations only in veins with endothelium from intact females. Results indicate that 17beta-estradiol causes acute endothelium-dependent relaxations in femoral veins. The relative contribution of nitric oxide and K(+) channels as mechanisms involved in relaxations to 17beta-estradiol in femoral veins is modulated by ovarian status.
authors.affiliation: Department of Physiology and Biophysics, Mayo Clinic and Foundation, Rochester, Minnesota 55905, USA.
authors.forename: M P
authors.initials: MP
authors.lastname: Bracamonte
authors.forename: M
authors.initials: M
authors.lastname: Jayachandran
authors.forename: K S
authors.initials: KS
authors.lastname: Rud
authors.forename: V M
authors.initials: VM
authors.lastname: Miller
mesh_terms: D000818:Animals; D015237:Dinoprost / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D004791:Enzyme Inhibitors / Q000494:pharmacology; D004958:Estradiol / Q000031:analogs & derivatives* / Q000494:pharmacology*; D005260:Female; D005268:Femoral Vein / Q000166:cytology / Q000187:drug effects* / Q000502:physiology*; D000077267:Fulvestrant; D007150:Immunohistochemistry; D066298:In Vitro Techniques; D010052:Ovariectomy; D026902:Potassium Channel Blockers / Q000494:pharmacology; D011960:Receptors, Estrogen / Q000037:antagonists & inhibitors; D013237:Stereoisomerism; D013552:Swine; D014661:Vasoconstriction / Q000187:drug effects / Q000502:physiology; D014664:Vasodilation / Q000187:drug effects / Q000502:physiology
chemical_list: D004791:Enzyme Inhibitors; D026902:Potassium Channel Blockers; D011960:Receptors, Estrogen; D000077267:Fulvestrant; D004958:Estradiol; D015237:Dinoprost