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Pituitary Ca2+ channels: blockade by conventional and novel Ca2+ antagonists.

We have identified several new agents that block Ca2+ channels in the rat pituitary GH4C1 cell line. These drugs, which include the diphenylbutylpiperidine antipsychotic pimozide, the calmodulin antagonist calmidazolium, and the steroidal Na+ channel toxin veratridine, were compared with several conventional Ca2+ antagonist in 45Ca2+ uptake, prolactin secretion, and whole cell patch voltage-clamp experiments. Pimozide, the most potent of these novel Ca2+ antagonists, inhibited depolarization-dependent 45Ca2+ uptake and prolactin secretion half maximally at a concentration of 100 nM, whereas calmidazolium and veratridine produced 50% inhibition at concentrations of 500 nM and 1 microM. In comparison, the three organic Ca2+ antagonists nitrendipine, verapamil, and diltiazem blocked 45Ca2+ uptake half maximally at concentrations of 2.5 nM, 1 microM, and 2.5 microM, respectively. All of the antagonists inhibited Ca2+ uptake and prolactin secretion stimulated by the dihydropyridine Ca2+ agonist BAY-K 8644 less potently than KCl-stimulated responses. In patch-clamp experiments, pimozide, veratridine, and nitrendipine blocked Ca2+ current through the slowly inactivating Ca2+ channels of GH4C1 cells. These results demonstrate that Ca2+ channels in an endocrine cell line can be blocked by a variety of molecules including sodium channel toxins and calmodulin antagonists. The data extend the pharmacological similarity between Ca2+ channels in pituitary and other excitable cells and suggest a structural similarity among several cellular proteins.