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Possible Involvement of Ryanodine Receptor-Mediated Intracellular Calcium Release in the Effect of Corticotropin-Releasing Factor on Adrenocorticotropin Secretion

Departments of Medicine (E.Y., M.Y., M.A., Y.O.) and Clinical Pathophysiology (Y.I., M.K., N.N.), Nagoya University Graduate School of Medicine and Hospital, Nagoya 466-8550, Japan; and Department of Medicine II (Y.O.), Hamamatsu University School of Medicine, Hamamatsu 431-3192, Japan

Abstract

We examined the role of intracellular calcium release in the regulation of CRH-induced ACTH secretion using the AtT20 corticotroph cell line. We found that ruthenium red, an inhibitor of ryanodine receptor, substantially diminished the secretory response, whereas Xestospongin C, an inositol 1,4,5-triphosphate receptor antagonist, had no effect. Expression of two ryanodine receptor subtypes (RyR1 and RyR3) was confirmed by RT-PCR. We also found that caffeine, a ryanodine receptor agonist, significantly stimulated, whereas thapsigargin, which causes depletion of intracellular calcium store, markedly diminished, the ACTH release. These results suggest that ryanodine receptor-mediated calcium-induced calcium release is involved in the regulation of CRH-induced ACTH release.

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