Estradiol enhances endothelium-dependent vasodilation via a nitric oxide pathway

Background and aim. The mechanisms by which estradiol dilates arterial vess els are still unclear. Our aim was to study if estradiol enhances endotheli um-dependent vasodilation in an experimental model of human arteries in vit ro, and if this effect is nitric oxide mediated. Methods. Using organ bath chambers, we studied 18 arterial rings obtained f rom left internal mammary arteries during coronary artery bypass grafting s urgery. Response to acetylcholine was evaluated at baseline and after the a ddition of estradiol 10(-6) mol/l to the medium, both in the presence or ab sence of a nitric oxide synthase inhibitor (L-NNA 10(-4) mol/l). Results. E stradiol significantly enhanced the relaxation of the arterial rings in res ponse to acetylcholine (52 +/- 20% after estradiol versus 42 +/- 22% at bas eline; n = 10; p = 0.02). However, endothelium-dependent vasodilation relax ation after estradiol addition was not enhanced in the presence of L-NNA (4 7 +/- 25% after estradiol versus 38 +/- 22% at baseline; n = 8; p = NS). Conclusions. Estradiol in vitro enhances endothelium-dependent vasodilation of internal human mammary artery rings; this effect is blunted after the a ddition to the medium of a nitric oxide inhibitor. Therefore, the vasodilat or properties of estradiol at the studied dosage depend on the nitric oxide pathway.