Secretion of luteinizing hormone (LH) and pituitary receptors for LH-releasing hormone as modified by the proestrous surge of progesterone

Abstract

Pituitary glands of proestrous (PRO) rats display enhanced LH secretory response to LHRH when compared to pituitary glands of estrous (EST) rats. In addition proestrous pituitary glands display a self-potentiating (priming) response to LHRH, whereas estrous pituitary glands do not. This study addresses the role of the proestrous surge of progesterone in converting the proestrous-like LH secretory responses of the pituitary gland to those of estrus. Anterior pituitary glands were obtained from PRO and EST rats. In addition, Pro rats were treated with pentobarbital alone (PRO/PB) or with pentobarbital plus progesterone (PRO/PB-P4). Pentobarbital was given to prevent proestrous surges of LH and progesterone. Pentobarbital-treated animals were killed the day after treatment, estrus. Pituitary glands from each group were tested for LH secretory response in a superfusion chamber with exposure of two 15-min pulses of 10 nM LHRH separated by 90 min, or assayed for LHRH receptor content using iodinated D-Ala6-LHRH. Anterior pituitary glands from PRO rats secreted higher levels of LH than EST rats in response to an LHRH pulse. Only PRO anterior pituitary glands secreted priming responses to LHRH. Though anterior pituitary glands obtained from pentobarbital-treated rats showed LH responses of similar magnitude to anterior pituitary glands of PRO rats after initial LHRH challenge, they did not display priming responses. Progesterone replacement (PRO/PB-P4) led to depressed secretory responses when compared to PRO pituitary glands similar to EST rats. LHRH receptor concentrations in pituitary glands of EST rats was lower than those in pituitary glands of PRO rats. Depression of pituitary LHRH receptor concentration from proestrus to estrus was prevented by pentobarbital-treatment on proestrus. Estrus-like depression of receptor concentration was restored after progesterone treatment (PRO/PB-P4). These data suggest the LHRH receptor depression on estrus is a consequence of the secretion of progesterone on proestrus. Further, the declining magnitude of the in vitro LH-secretory response to LHRH follows a declining LHRH receptor concentration; however no correlation exists between receptor number and ability to prime.