Different mechanisms for testosterone-induced relaxation of aorta between normotensive and spontaneously hypertensive rats

The tension in isolated ring preparations of the thoracic aortae from Wista r-Kyoto rats (WKY) and spontaneously hypertensive rats (SHR) was measured i sometrically to study the differences in testosterone-induced relaxation be tween WKY and SHR aortic rings. Testosterone (9 to 300 mu mol/L) induced a concentration-dependent relaxation in both WKY and SHR aortic rings, and th e relaxation induced by testosterone was greater in SHR than WKY. The relax ation induced by testosterone was significantly reduced by denudation of en dothelium in SHR but not WKY. Indomethacin, an inhibitor of cyclooxygenase, and N-G-nitro-L-arginine, an inhibitor of nitric oxide (NO) synthase, show ed Little influence on the relaxation induced by testosterone in both WKY a nd SHR aortic rings. Glibendamide, a selective inhibitor of ATP-sensitive p otassium channels, significantly reduced the relaxation induced by testoste rone in both WKY and SHR aortic rings, although the extent of reduction was greater in WKY than SHR. On the other hand, 4-aminopyridine, a selective i nhibitor of voltage-dependent potassium channels, and tetraethylammonium, a n inhibitor of calcium-activated potassium channels, significantly reduced the relaxation induced by testosterone in SHR but not WKY. These results su ggest that the mechanisms of testosterone-induced vasorelaxation in both WK Y and SHR involve, in part, ATP-sensitive potassium channels in the thoraci c aortae and that in SHR aortic rings, testosterone may release endothelium -derived substances that may cause hyperpolarization of the cells by a mech anism that involves potassium channels. Moreover, the data show differences between WKY and SHR in the function of ATP-sensitive, voltage-dependent, a nd calcium-activated potassium channels.