Conrad K P, Mosher M D, Brinck-Johnsen T, Colpoys M C
Department of Physiology, University of New Mexico School of Medicine, Albuquerque 87131.
Am J Physiol. 1994 Apr;266(4 Pt 2):R1267-72. doi: 10.1152/ajpregu.1994.266.4.R1267.
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.
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（如大鼠）正常妊娠的一个持续特征。然而，这种生理适应的机制仍不确定。由于在怀孕期间，17β-雌二醇（E2）和孕酮（P）的血浆水平显著升高，我们检验了这些激素可能介导降压反应降低的假设。在双侧卵巢切除和对大鼠进行慢性仪器植入7天后，分别在间隔≥48小时的两个时间点测试精氨酸加压素、血管紧张素II和去甲肾上腺素的升压反应。然后通过皮下植入21天缓释类固醇丸剂给予E2、P或E2与P的组合。在整个类固醇治疗期间的不同时间再次测试升压反应。通过放射免疫测定评估类固醇的血浆浓度，并给予接近和超过我们实验室中妊娠大鼠循环水平的激素剂量。尽管血浆E2和/或P长期升高，但在任何类固醇治疗方案中，我们均未观察到升压反应性的持续减弱，也未观察到平均动脉压下降，而这在妊娠后期的大鼠中通常会出现。总之，我们无法支持E2和/或P导致大鼠妊娠时升压反应性降低的假设。
