The role of calcium in gonadotropin-releasing hormone induction of follicle-stimulating hormone release by the pituitary gonadotrope.

Binding of gonadotropin-releasing hormone (GnRH) to the pituitary gonadotrope induces activation of a membrane associated calcium channel, resulting ultimately in luteinizing hormone release. The role of calcium mobilization in GnRH-induced follicle-stimulating hormone (FSH) release was explored using anterior pituitary glands from female rats in a perifusion tissue culture system. While perifusion with GnRH (10 ng/ml) induced a constant level of gonadotropin release, the calcium channel blocker verapamil (10(-4)M) depressed FSH release, as did dantrolene (10(-4)M), an antagonist of intracellular calcium mobilization. When the calcium ionophore A23187 (10(-5) M) was substituted for GnRH, FSH release was not only maintained but increased. Antagonism of the activity of calmodulin (CAM) with trifluoperazine (10(-4)M), however, did not depress FSH release. Cellular content of cAMP and cGMP increased in response to GnRH. When FSH secretion was ionophoretically induced by A23187, however, little cAMP was detected. These results support a role for calcium mobilization in the second messenger cascade underlying GnRH-induced FSH release. The role for calcium in the disparate release of FSH and LH were further discussed in the context of these data.