Binding of human chorionic gonadotropin and response of cyclic nucleotides to luteinizing hormone in luteal tissue from rats treated with prostaglandin F2alpha.

Prostaglandin F2alpha (PGF2alpha) caused a marked and highly reproducible fall of over 85% (P less than .001) in serum progesterone and in the capacity of luteal tissue to bind hCG, within 30 h. No change in the affinity of the receptor for iodinated hCG was observed. The addition of LH (1 mug/ml) to incubation flasks containing luteal tissue slices from both control and PGF2alpha-treated animals caused a significant stimulation of progesterone output in the control (P less than .05), but not in tissue previously exposed to PGF2alpha in vivo. Indeed, progesterone output by the latter tissue was severely reduced independent of the presence of LH. Although cAMP content was significantly elevated in luteal tissue incubated with LH (P less than .01), the degree of stimulation of cAMP by LH was reduced 35% (P less than .05) in luteal tissue from rats treated with PGF2alpha. The content of cGMP was generally reduced by addition of LH to the incubation media, by pretreatment of the animals with PGF2alpha, and by incubation alone. This study shows that luteolysis induced by PGF2alpha is accompanied by a loss in gonadotropin receptor, a conclusion supported by the loss in LH stimulation of cAMP and progesterone synthesis.