Effects of 17 beta-estradiol and progesterone on pressor responses in conscious ovariectomized rats.
Effects of 17 beta-estradiol and progesterone on pressor responses in conscious ovariectomized rats.
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17β-雌二醇和黄体酮对清醒卵巢切除大鼠升压反应的影响。
DOI：
10.1152/ajpregu.1994.266.4.r1267
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发表时间：
1994
期刊：
影响因子：
--
通讯作者：
Colpoys,MC
中科院分区：
文献类型：
--
作者：
Conrad,KP;Mosher,MD;Brinck-Johnsen,T;Colpoys,MC
对几种给予的血管收缩剂的升压反应性减弱是人类和其他物种（例如大鼠）正常妊娠的一个恒定特征。然而，这种生理适应的机制仍不确定。由于 17β-雌二醇 (E2) 和孕酮 (P) 的血浆水平在怀孕期间显着增加，因此我们测试了这些激素可能介导降压反应减少的假设。对大鼠进行双侧卵巢切除和长期器械治疗后 7 天，两次测试精氨酸加压素、血管紧张素 II 和去甲肾上腺素的升压反应，两次时间间隔 > 或 = 48 小时。然后通过皮下植入21天释放的类固醇颗粒来施用E2、P或E2和P的组合。在类固醇治疗期间的不同时间再次测试升压反应。通过放射免疫测定法评估类固醇的血浆浓度，所给予的激素剂量接近并超过我们实验室针对妊娠大鼠发现的循环水平。尽管血浆 E2 和/或 P 长期升高，但我们没有观察到任何类固醇治疗方案中升压反应性的一致减弱，也没有观察到平均动脉压的下降，这通常在妊娠后期的大鼠中发现。总之，我们无法支持 E2 和/或 P 导致大鼠妊娠升压反应性减弱的假设。
Attenuation of pressor responsiveness to several administered vasoconstrictors is a constant feature of normal gestation in humans and other species, such as the rat. However, the mechanism of this physiological adaptation remains uncertain. Because plasma levels of 17 beta-estradiol (E2) and progesterone (P) increase markedly during pregnancy, we tested the hypothesis that these hormones may mediate the reduced pressor responses. Seven days after bilateral ovariectomy and chronic instrumentation of rats, the pressor responses of arginine vasopressin, angiotensin II, and norepinephrine were tested on two occasions > or = 48 h apart. Then E2, P, or a combination of E2 and P was administered by subcutaneous implantation of 21-day-release steroid pellets. Pressor responses were again tested at various times throughout the period of steroid treatment. The plasma concentrations of the steroids were assessed by radio-immunoassay, and doses of the hormones were given that both approximated and exceeded circulating levels found in our laboratory for gravid rats. Despite chronic elevation of plasma E2 and/or P, we did not observe consistent attenuation of pressor responsiveness in any of the steroid-treatment regimens, nor was a decline in mean arterial pressure observed, which is typically found in rats during late gestation. In conclusion, we are unable to support the hypothesis that E2 and/or P contributes to the diminished pressor responsiveness of rat pregnancy.