Pergamon Life Sciences, Vol. 57, No. 5, pp. 473-486, 1995 Copyright 0 1995 Elsevier Science Ltd Printed in the USA. All rights reserved @x4-3205/9s $9.50 + .oo 0024-3205(95)00281-2 EFFECTS OF ACUTE AND CHRONIC ESTROGENIC TREATMENT ON VASOMOTOR RESPONSES OF AORTIC RINGS FROM OVARIECTOMUED RATS M.C. Paredes-Carbajal, M.A. Jukez-Oropeza*, C.M. Ortiz-Mendoza and D. Mascher Department of Physiology and *Department of Biochemistry, School of Medicine, II.N.A.M., P.O. Box 70-250, Mexico D.F. 04510, MEXICO (Received in final form May 8, 1995) Summary The effects of either chronic or acute estrogenic treatment on the “in vitro” vasomotor responses to phenylephrine (1 Oe9- 10.’ M) and to carbachol ( 1 OS“‘- 10.’ M) of aortic rings excised from ovariectomized rats were analyzed Chronic estrogenic treatment consisted in a single subcutaneous dose of 1 umol estradiol 17-stearate. Effects of acute estrogenic treatment were evaluated by recording the responses of aortic rings excised from untreated ovariectomized rats both before and after the addition of 17l3- estradiol to the superfUsing solutions. In order to identify the endothelium-dependent responses each experiment was performed simultaneously on pairs of rings from the same aorta, one with and the other without functional endothelium. The contractile responses to phenylephrine of endothelium-intact vessels were attenuated by chronic estrogenic treatment; this attenuation was mrther increased by preincubation of the vessels with indomethacin and was reverted by No-nitro-L-arginine methyl ester. Either chronic or acute estrogenic treatment enhanced the carbachol-induced endothelium dependent relaxation of phenylephrine-precontracted rings. The results may be explained by assuming that estrogens increase the basal release of both nitric oxide and a cyclooxygenase-dependent vasoconstricting prostanoid as well as the receptor-mediated release of nitric oxide from the endothelium of the rat aorta. Kq Wotds: endothelium, estrogens, nitric oxide, prostanoids, aortic rings Women in the reproductive age have a lower prevalence of atherosclerosis related diseases than age matched men (1,2). This difference decreases after both surgical and natural menopause and postmenopausal women are at a much higher risk of developing coronary artery disease than premenopausal women of similar age (3,4). On the other hand, estrogen replacement therapy lowers the incidence of atherosclerotic diseases in ovariectomized and postmenopausal women (5-9). The beneficial effects of estrogens are even greater in women with already existing atherosclerotic disease (IO). Based on these epidemiological observations a “protective” role of estrogens, preventing atherosclerotic vascular diseases has been postulated. Several mechanisms by which this protection may be achieved have been proposed (5, 11-l 5). In the last few years, it has become evident that Corresponding author: Ma. Cristina Paredes-Carbajal. Department of Physiology, School of Medicine, U.N.A.M., P.O. Box 70-250, Mexico D.F. 045 10, MEXICO. FAX (525) 623-224 I E-mail majo@servidor.dgsca.unam.mx.