Differences in the mechanisms for relaxation of aorta induced by 17beta-estradiol or progesterone between normotensive and hypertensive rats.

The tension in isolated ring preparations of the thoracic aorta from Wistar-Kyoto rats (WKY) and spontaneously hypertensive rats (SHR) was measured isometrically to study if there are any differences in the mechanisms of 17beta-estradiol- or progesterone-induced relaxation between WKY and SHR aortic rings. 17beta-Estradiol and progesterone caused dose-dependent vascular relaxation of the thoracic aorta precontracted with norepinephrine in both WKY and SHR, and the relaxation induced by 17beta-estradiol was greater in SHR than WKY. However, no difference was observed in progesterone-induced relaxation between SHR and WKY. With the exception of tetraethylammonium, an inhibitor of Ca(2+)-activated K(+) channels, glibenclamide, a selective inhibitor of ATP-sensitive K(+) channels, or 4-aminopyridine, a selective inhibitor of voltage-dependent K(+) channels, significantly reduced 17beta-estradiol-induced relaxation only in SHR, but not in WKY. Both 17beta-estradiol and progesterone inhibited Ca(2+)-induced vasocontraction of the thoracic aorta in K(+) depolarization medium in WKY and SHR. These results suggest that the mechanisms of 17beta-estradiol-induced relaxation in SHR aorta are at least partially mediated via ATP-sensitive and voltage-sensitive K(+) channels in addition to the inhibition of Ca(2+) channels, although those of progesterone-induced relaxation in both WKY and SHR are mainly concerned with the inhibition of Ca(2+) channels rather than the operation of K(+) channels. Moreover, a difference in 17beta-estradiol-induced relaxation between WKY and SHR aorta suggests a possibility that vascular response in SHR is modified by hypertension.