Vascular effects of estrone and diethylstilbestrol in porcine coronary arteries

Abstract

OBJECTIVE: To explore the effects of different estrogens on vascular function, we compared the vasorelaxant effects of 17β2-estradiol, 17β±-estradiol, estrone, and the synthetic estrogen diethylstilbestrol (DES) on porcine coronary arterial segments. DESIGN: Porcine coronary arterial rings were contracted with the stable thromboxane A2 analogue U46619 (3 × 10 M), and direct relaxation was examined by the addition of increasing concentrations of 17β2-estradiol, 17β±-estradiol, estrone, or DES (10 to 10 M). Modulation of agonist-induced contraction and relaxation was studied in coronary arterial rings incubated for 20 minutes with DES or estrone (10-10 M) with 17β2-estradiol (10 M) as comparison. RESULTS: Direct relaxation of arterial rings potentiated by these estrogens was recorded with a rank order potency of DES > 17β2-estradiol > estrone > 17β±-estradiol. 17β2-Estradiol potentiated relaxation responses to sodium nitroprusside and levcromakalim but not bradykinin or A23187 while reducing contractions to 5-hydroxytryptamine and U46619. DES and estrone, both at 10 M, mimicked the 17β2-estradiol-potentiated sodium nitroprusside and levcromakalim relaxation responses. Additionally, the inhibitory effects of 17β2-estradiol (10 M) on 5-hydroxytryptamine- and U46619-induced contractions were partially reproducible by DES (10 M) and estrone (10 M). CONCLUSIONS: Although DES is the most potent among the tested estrogenic compounds in eliciting relaxation, 17β2-estradiol is more effective than estrone and DES at enhancing endothelium-independent relaxation and reducing vascular contraction in porcine coronary arteries. Copyright © 2009 The North American Menopause Society.