Corpus Luteum Function and Adenylyl Cyclase Stimulability in the Rat after an Estradiol Benzoate-Induced Ovulatory Surge of Luteinizing Hormone: Role of Prolactin*

Abstract

Estradiol benzoate (E; 20 μg, sc) was given on diestrus day 1 to 4-day cycling rats to advance the ovulatory LH surge by 1 day. Estrogen treatment is known to result in the maintenance of two apparently functional sets of corpora lutea (CL). Previously, our laboratory has demonstrated that E treatment results in the maintenance of LH-stimulable adenylyl cyclase activity in the 4-day-old CL on the day of expected proestrus. We investigated whether the effect of E was mediated by PRL by using an eryocryptine analog CB-154 to inhibit PRL release. We measured LH- and isoproterenol (Iso)-stimulable adenylyl cyclase activity and progesterone levels in 4- and 1-day-old CL and progesterone levels in serum. Iso was used as a control hormone to monitor receptor-mediated regulation of adenylyl cyclase activity. Progesterone was measured by RIA to examine whether LH-stimulable adenylyl cyclase activity correlated with CL function. We found that E treatment resulted in increased LH-stimulable adenylyl cyclase activity and elevated luteal progesterone in the 4-day-old CL when compared to control CL; serum progesterone was also elevated after E treatment. CB-154 plus E treatment prevented the elevation of tissue and serum progesterone and prevented the increase in LH stimulability of adenylyl cyclase activity in 4-day-old CL. PRL plus CB-154 plus E reversed the effect of CB-154 plus E and resulted in increased LH stimulability of CL cyclase and in elevated tissue and serum progesterone. LH-stimulable adenylyl cyclase activity and tissue progesterone content were low in all 1-day-old CL. Interestingly, Iso-stimulable adenylyl cyclase activity was high (8- to 10-fold) in all 4-day-old CL. We confirm that E treatment 1) advanced the LH surge and ovulation by 1 day, 2) resulted in pseudopregnancy, and 3) maintained LH-stimulable adenylyl cyclase activity after a desensitizing LH surge. We conclude that PRL is part of the means by which estrogen acts to maintain LH-stimulable adenylyl cyclase activity and functionality in 4-day-old CL. (Endocrinology106: 382, 1980)