Mechanisms for Vascular Effects of Androgens in Normotensive and Hypertensive Rats

Castration had no effect on baseline BP and vascular sensitivity to acetylcholine and deficiency of nitric oxide and prostacyclin in normotensive specimens. Castration of hypertensive specimens decreased BP and potentiated the hypotensive effects of acetylcholine, but did not modulate vascular sensitivity to the blockade of nitric oxide and prostacyclin synthesis. The removal of the testicles abolished the pressor influence of glybenclamide in hypertensive and, particularly, in normotensive males. These data indicate that the non-endothelial vascular effects of androgens (i.e., stimulation of K(ATP) channels) predominate under normal conditions. The activating effects of androgens on K(ATP) channels decrease during hypertension, which is accompanied by inhibition of endothelium-dependent vasorelaxation. The production of nitric oxide and prostacyclin remains unchanged under these conditions. Our results suggest that endothelium-derived hyperpolarizing factor is involved in these processes.