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  • Title: Vascular effects of 17 beta-estradiol in male Sprague-Dawley rats.
    Author: Shan J, Resnick LM, Liu QY, Wu XC, Barbagallo M, Pang PK.
    Journal: Am J Physiol; 1994 Mar; 266(3 Pt 2):H967-73. PubMed ID: 8160845.
    Abstract:
    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.
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