Acetylcholine-mediated relaxation in rat thoracic aorta is enhanced following acute exposure to physiological concentrations of 17 beta-estradiol

We investigated the effects of short-term exposure to low concentrations of 17 beta-estradiol on vasorelaxation using an in vitro rat thoracic aortic ring preparation. Supraphysiological levels of 17 beta-estradiol directly r elaxed phenylephrine-contracted rings. Although acute incubation (20 min) w ith 1-100 nM of the female sex hormone did not have any significant effect on phenylephrine-contracted rings, relaxation evoked by acetylcholine was s ignificantly potentiated. In contrast, calcium ionophore A23187-elicited en dothelium-dependent relaxation as well as cromakalim- and sodium nitropruss ide-mediated endothelium-independent relaxation was unchanged following the same regime with 17 beta-estradiol. These results demonstrate that short-t erm treatment with physiologically relevant levels of 17 beta-estradiol, wh ich on their own have no effect, enhances endothelium-dependent relaxation by acetylcholine. The vascular effects observed herein may partly account f or some of the improved acute vasodilatory responses reported with 17 beta- estradiol on blood flow in humans.