Abstract
An early event of the decidual cell reaction in response to either natural or artificial deciduogenic stimuli is an increase in the activity of alkaline phosphatase in endometrial stromal cells. Since it is known that prostaglandins have a stimulatory role in other events of the decidual cell reaction, this study addressed whether prostaglandins have any role in the increase in alkaline phosphatase activity. Mature ovariectomized rats were sensitized for the decidual cell reaction with s.c. injections of estrogen and progesterone. To investigate the effect of inhibition of endogenous prostaglandin synthesis, rats received indomethacin (s.c. and via intrauterine infusion) or the vehicles sesame oil and phosphate-buffered saline with gelatin. Biochemical measurement of endometrial alkaline phosphatase activity and protein content revealed that, compared to the controls, indomethacin had no significant effect at 24 h after the initiation of infusion. At 48 h, unit activity (activity per unit protein) and total activity were substantially lower in indomethacin-treated than in vehicle-treated rats. At 72 h, there was a less dramatic difference between the unit activities of the two groups; however, there was a 10-fold difference between the total measureable activities of the two groups. Infusion of exogenous prostaglandins PGE2 or PGF2.alpha. into rats treated with indomethacin overrode the inhibitory effect of indomethacin upon the increase in alkaline phosphatase activity. The dose-response relationshp indicated that both PGE2 and PGf2.alpha. have the same efficacy. In rats that had been treated similarly, localization of uterine alkaline phosphatase activity by histochemistry demonstrated a high correlation between the histochemical and biochemical data. It is concluded that prostaglandins are involved in a causative manner in the increase in uterine alkaline phosphatase activity during decidualization.