Vol. 283, Issue 6, H2389-H2396, December 2002
Acute effects of 17
-estradiol on femoral veins from adult
gonadally intact and ovariectomized female pigs
M. P.
Bracamonte1,
M.
Jayachandran2,
K. S.
Rud2, and
V.
M.
Miller1,2
1 Departments of Physiology and Biophysics, and
2 Surgery, Mayo Clinic and Foundation, Rochester,
Minnesota 55905
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
9 to 105 M) were obtained in veins
contracted with prostaglandin F2
in the absence and
presence of inhibitors of either estrogen receptors (ICI-182780;
105 M), nitric oxide synthase
[NG-monomethyl-L-arginine
(L-NMMA); 104 M], soluble guanylate cyclase
(1-H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one; 105 M), or potassium channels (tetraethylammonium;
102 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[4,3-a]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+ channels as mechanisms involved in relaxations to
17-estradiol in femoral veins is modulated by ovarian status.
endothelium; hyperpolarizing factor; nitric oxide; potassium
channels
