Role of calcium in acute stimulated release of prolactin from neoplastic GH3 cells

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Abstract
Using a Ca-sensitive electrode to monitor Ca movements, neoplastic GH3 cells experienced a net accumulation of Ca when exposed to elevated (50 mM) K+. Acute prolactin (PRL) release was also stimulated under these conditions. Both Ca uptake and PRL release could be blocked by the Ca antagonist methoxyverapamil (D-600). Thyrotropin-releasing hormone (TRH) also stimulated PRL release but had no effect on cellular Ca accumulation. Likewise, D-600 had no effect on TRH-induced PRL release. Enhanced secretory activity apparently does not require an increase in intracellular Ca content. The observation that secretagogues do not stimulate PRL release in the absence of extracellular Ca was investigated. When GH3 cells were placed in a Ca-free medium, they underwent a prompt and sustained loss of cellular Ca. The loss of such intracellular Ca could be blocked with D-600. The inability of TRH to stimulate the release of PRL in Ca-free medium is due to the loss of intracellular Ca and not to the absence of external Ca per se.