Synthesis and Release of Luteinizing Hormonein Vitroby Rat Anterior Pituitary Cells: Effects of Gallopamil Hydrochloride (D600) and Pimozide*

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Abstract
We compared the role of Ca2+ in regulating GnRH-induced LH synthesis and release from cultured rat pituitary cells. LH synthesis and release were measured after a 4-h treatment of cells with gallopamil hydrochloride (D600; 1 and 100 μM), a Ca2+ channel blocker, or pimozide (0.5 and 5.0 μM), a calmodulin inhibitor, with or without 1 nm GnRH. LH translation and glycosylation were monitored by measuring incorporation of [14C]alanine and [3H]glucosamine, respectively, into total (cell and medium) immunoprecipitable LH. GnRH significantly (P < 0.01) increased total [3H]LH (glycosylation), but had no effect on total [14C]LH (translation). D600 significantly (P < 0.01) depressed (1 HM) and completely blocked (100 μM) GnRH-induced LH glycosylation and release of [3H]LH, [14C]LH, and immunoreactive LH. D600 (100 μM) also reduced (P < 0.05) total basal synthesis of [14C]LH. Neither dose of D600 altered uptake of [3H]glucosamine, but 100 μM D600 significantly (P < 0.01) depressed its incorporation into total protein. D600 (100 μM) significantly (P < 0.01) depressed [14C] alanine uptake and incorporation into total protein. Pimozide significantly (P < 0.01) reduced, in a dose-related manner, GnRH-induced LH glycosylation, and release of immunoreactive LH, [3H]LH, and [14C]LH. Pimozide did not alter LH translation or uptake of radiolabeled precursors or their incorporation into total protein. These results demonstrate that D600 and pimozide inhibit both GnRH-induced LH glycosylation and release. Thus, the actions of GnRH on LH glycosylation and release are both mediated by similar Ca2+-dependent pathways. (Endocrinology117: 1608–1614, 1985)

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