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

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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 17β-estradiol- or progesterone-induced relaxation between WKY and SHR aortic rings. 17β-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 17β-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 17β-estradiol-induced relaxation only in SHR, but not in WKY. Both 17β-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 17β-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 17β-estradiol-induced relaxation between WKY and SHR aorta suggests a possibility that vascular response in SHR is modified by hypertension.