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An investigation of the involvement of calcium in the control of prolactin secretion: studies with low calcium, methoxyverapamil, cobalt and manganese.

The possible role of calcium as a primary mediator in the control of prolactin secretion from normal pituitary cells was examined. Basal prolactin secretion, and secretion stimulated by thyrotrophin releasing hormone (TRH), raised K+ or the calcium ionophore, A23187, were all dependent on the presence of extracellular Ca2+. The calcium channel antagonists, methoxyverapamil, cobalt and manganese, inhibited basal, TRH- and K+-stimulated prolactin secretion. In addition, prolactin secretion stimulated by a phosphodiesterase inhibitor, isobutylmethylxanthine, which increases cellular cyclic AMP, was inhibited by these Ca2+ antagonists. These observations indicate that Ca2+ may be the primary intracellular mediator in the control of prolactin secretion, with cyclic AMP having a secondary modulatory role on Ca2+ influx, probably on voltage-dependent Ca2+ channels.