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

Attenuation of presser responsiveness to several administered vasocons trictors is a constant feature of normal gestation in humans and other species, such as the rat. However, the mechanism of this physiologica l adaptation remains uncertain. Because plasma levels of 17 beta-estra diol (E(2)) and progesterone (P) increase markedly during pregnancy, w e tested the hypothesis that these hormones may mediate the reduced pr esser responses. Seven days after bilateral ovariectomy and chronic in strumentation of rats, the presser responses of arginine vasopressin, angiotensin II, and norepinephrine were tested on two occasions greate r 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 ho rmones were given that both approximated and exceeded circulating leve ls 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 w as a decline in mean arterial pressure observed, which is typically fo und in rats during late gestation. In conclusion, we are unable to sup port the hypothesis that E(2) and/or P contributes to the diminished p resser responsiveness of rat pregnancy.