EFFECTS OF 17-BETA-ESTRADIOL AND PROGESTERONE ON PRESSER RESPONSES IN CONSCIOUS OVARIECTOMIZED RATS

Attenuation of presser 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 (E(2)) and progesterone (P) increase markedly during pregnancy, we tested the hypothesis that these hormones may mediate the reduced presser responses. Seven days after bilateral ovariectomy and chronic instrumentation of rats, the presser responses of arginine vasopressin, angiotensin II, and norepinephrine were tested on two occasions greater than or equal to 48 h apart. Then E(2), P, or a combination of E(2) and P was administered by subcutaneous implantation of 21-day-release steroid pellets. Presser responses were again tested at various times throughout the period of steroid treatment. The plasma concentrations of the steroids were assessed by radioimmunoassay, 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 E(2) and/or P, we did not observe consistent attenuation of presser 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 E(2) and/or P contributes to the diminished presser responsiveness of rat pregnancy.