Shan J, Resnick L M, Liu Q Y, Wu X C, Barbagallo M, Pang P K
Department of Physiology, University of Alberta, Edmonton, Canada.
Am J Physiol. 1994 Mar;266(3 Pt 2):H967-73. doi: 10.1152/ajpheart.1994.266.3.H967.
Bolus intravenous injections of 100 micrograms/kg 17 beta-estradiol significantly decreased the pressor responses to norepinephrine (NE; 0.3 microgram/kg) at the fourth, fifth, and sixth hour in anesthetized male Sprague-Dawley rats. At doses of 10(-6) to 3 x 10(-5) M, 17 beta-estradiol relaxed the sustained phase of contraction in male Sprague-Dawley rat tail artery helical strips precontracted in vitro by [Arg8]vasopressin (AVP), KCl, or NE. The effect was dose dependent. At doses of 3 x 10(-6) to 3 x 10(-5) M, it also decreased the initial phase of tension generation and extracellular Ca(2+)-dependent vasoconstriction induced by NE, AVP, or KCl in a dose-dependent manner in male Sprague-Dawley rat tail artery helical strips. 17 beta-Estradiol (2 x 10(-8) to 2 x 10(-6) M) decreased the voltage-dependent inward Ca2+ current and the intracellular free Ca2+ concentration ([Ca2+]i) increment induced by 15 mM KCl in a dose-dependent manner (3.6 x 10(-8) to 3.6 x 10(-6) M) in vascular smooth muscle cells (VSMC) isolated from male Sprague-Dawley rat tail arteries. We suggest that, at pharmacological doses, estrogen has a direct vasodilating effect on the rat tail artery that is mediated by its inhibitory effect on Ca2+ influx through voltage-dependent Ca2+ channels. The inhibitory effect of estrogen on the pressor responses to NE or AVP may be correlated with its modulation of VSMC [Ca2+]i through its actions on membrane Ca2+ channels.
在麻醉的雄性斯普拉格 - 道利大鼠中，静脉推注100微克/千克的17β - 雌二醇在第四、第五和第六小时显著降低了对去甲肾上腺素（NE；0.3微克/千克）的升压反应。在10^(-6)至3×10^(-5)M的剂量下，17β - 雌二醇使体外预先由[精氨酸8]血管加压素（AVP）、氯化钾或去甲肾上腺素预收缩的雄性斯普拉格 - 道利大鼠尾动脉螺旋条带的收缩持续期松弛。该作用呈剂量依赖性。在3×10^(-6)至3×10^(-5)M的剂量下，它还以剂量依赖性方式降低了雄性斯普拉格 - 道利大鼠尾动脉螺旋条带中由去甲肾上腺素、血管加压素或氯化钾诱导的张力产生初始阶段和细胞外钙（Ca(2+)）依赖性血管收缩。17β - 雌二醇（2×10^(-8)至2×10^(-6)M）以剂量依赖性方式（3.6×10^(-8)至3.6×10^(-6)M）降低了从雄性斯普拉格 - 道利大鼠尾动脉分离的血管平滑肌细胞（VSMC）中由15 mM氯化钾诱导的电压依赖性内向钙电流和细胞内游离钙浓度（[Ca(2+)]i）增加。我们认为，在药理剂量下，雌激素对大鼠尾动脉具有直接的血管舒张作用，这是由其对通过电压依赖性钙通道的钙内流的抑制作用介导的。雌激素对去甲肾上腺素或血管加压素升压反应的抑制作用可能与其通过对膜钙通道的作用调节VSMC [Ca(2+)]i有关。
