CALCITONIN DECREASES THYROTROPIN-RELEASING HORMONE-STIMULATED PROLACTIN-RELEASE THROUGH A MECHANISM THAT INVOLVES INHIBITION OF INOSITOL PHOSPHATE PRODUCTION

Calcitonin is present in both the hypothalamus and pituitary of the rat, and normal rat anterior pituitary cells express calcitonin receptors. Calcitonin has been reported to inhibit or to stimulate PRL release from rat anterior pituitary cells. We have investigated the effects of salmon calcitonin on basal and stimulated PRL release from rat anterior pituitary cells and have studied the effects of this peptide on the intracel-lular biochemical pathways involved in PRL release. Salmon calcitonin had no significant effect on basal PRL release, but inhibited (P < 0.01) TRH-stimulated PRL release without af-fecting PRL release promoted by angiotensin II, neurotensin, phorbol myristate acetate (a protein kinase C activator), or maitotoxin (a calcium channel activator). Salmon calcitonin had no effect on the increase in PRL release and intracellular cAMP concentration after exposure of pituitary cells to vasoactive intestinal peptide or forskolin. Salmon calcitonin significantly decreased (P < 0.01) the TRH-stimulated rise in inositol phos-phates without affecting the angiotensin II-stimulated increase in inositol phosphates. Similarly, salmon calcitonin decreased the TRH-stimulated increase in cytosolic calcium and arachi- donate liberation by pituitary cells. We conclude that salmon calcitonin selectively decreases TRH-stimulated PRL release by a mechanism that involves a decrease in inositol phosphate production, as well as a subsequent reduction in cytosolic cal-cium levels and in arachidonate liberation. © 1990 by The Endocrine Society.