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Articles in PresS, published online ahead of print September 12, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00184.2002
Submitted on March 4, 2002
Accepted on August 15, 2002
1 Department s of Physiology and Biophysics, Mayo Clinic and Foundation, Rochester, MN, USA
2 Department of Surgery, Mayo Clinic and Foundation, Rochester, MN, USA
3 Department s of Physiology and Biophysics, Mayo Clinic and Foundation, Rochester, MN, USA; Department of Surgery, Mayo Clinic and Foundation, Rochester, MN, USA
* To whom correspondence should be addressed. E-mail: miller.virginia{at}mayo.edu.
Experiments were designed to determine acute effects of 17ß-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 17ß-estradiol (10-9 to 10-5M) were obtained in veins contracted with prostaglandin F2
in the absence and presence of inhibitors of either estrogen receptors (ICI 182, 780; 10-5M), nitric oxide synthase (L-NMMA; 10-4M), soluble guanylate cyclase, [1-H-(1.2.4) oxadiazolo (4,3-A) quanoxalin (ODQ; 10-5M)], or potassium channels (tetraethylammonium, TEA, 10-2M). Estrogen receptors were identified by Western blotting and immunostaining in veins of both groups. 17ß-estradiol caused acute, endothelium-dependent relaxations in both groups. Relaxations to 17ß-estradiol were inhibited by L-NMMA and ODQ but not ICI 182,780. TEA only inhibited relaxations in veins with endothelium from intact females. Results indicate that 17ß-estradiol causes acute endothelium-dependent relaxations in femoral veins. Relative contribution of nitric oxide and potassium channels as mechanisms involved in relaxations to 17ß-estradiol in femoral veins are modulated by ovarian status.
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