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

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