title: Differences in the mechanisms for relaxation of aorta induced by 17beta-estradiol or progesterone between normotensive and hypertensive rats.
abstract: 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.
authors.affiliation: Department of Pharmacology, Tokyo University of Pharmacy and Life Science, 1432-1, Horinouchi, Hachioji, Tokyo 193-0392, Japan.
authors.forename: Tamao
authors.initials: T
authors.lastname: Unemoto
authors.forename: Hideo
authors.initials: H
authors.lastname: Honda
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Kogo
mesh_terms: D000818:Animals; D001013:Aorta, Thoracic / Q000187:drug effects; D002121:Calcium Channel Blockers / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D004958:Estradiol / Q000494:pharmacology*; D066298:In Vitro Techniques; D008297:Male; D009119:Muscle Contraction / Q000187:drug effects; D009131:Muscle, Smooth, Vascular / Q000187:drug effects*; D009638:Norepinephrine / Q000494:pharmacology; D026902:Potassium Channel Blockers / Q000494:pharmacology; D011374:Progesterone / Q000494:pharmacology*; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY; D011987:Receptors, Steroid / Q000037:antagonists & inhibitors; D014664:Vasodilation / Q000187:drug effects*
chemical_list: D002121:Calcium Channel Blockers; D026902:Potassium Channel Blockers; D011987:Receptors, Steroid; D011374:Progesterone; D004958:Estradiol; D009638:Norepinephrine