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Role of calcium in the thyrotropin-releasing hormone-stimulated release of prolactin from pituitary cells in culture.
Authors:A H Tashjian  M E Lomedico  D Maina
Institution:1. Laboratory of Pharmacology, Harvard School of Dental Medicine, Boston, MA 02115 USA;2. Department of Pharmacology, Harvard Medical School, Boston, MA 02115 USA
Abstract:Thyrotropin-releasing hormone (TRH) or 50 mM K+ stimulated the acute release of prolactin from the GH4C1 strain of rat pituitary cells in culture. The enhanced release of prolactin was inhibited in a dose-related manner by the Ca+2 antagonist Co+2 (2.0 to 0.5 mM) as well as by the Ca+2 chelator EGTA (1.0 mM). Co+2 also reduced spontaneous basal prolactin release. There was partial reversal of the inhibitory effect of Co+2 (2.0 mM) by Ca+2 (2.0 mM) and complete reversal of the inhibitory effect of EGTA (1.0 mM) by Ca+2 (2.0 mM). The enhanced release of prolactin stimulated by 50 mM K+ was maximal by 10–20 minutes in medium containing 0.67 to 0.74 mM Ca+2. Na+ (50 mM) did not mimic the effect of high K+. We conclude that Ca+2 is an essential cation in mediating the actions of high external K+ and TRH on the release of prolactin by GH4C1 cells.
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