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Cell-Type Specific Messenger Functions of Extracellular Calcium in the Anterior Pituitary

Dragoslava Zivadinovic, Melanija Tomi, Davy Yuan and Stanko S. Stojilkovic

Endocrinology and Reproduction Research Branch, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 20892-4510

Address all correspondence and requests for reprints to: Dr. Stanko Stojilkovic, Section on Cellular Signaling, Endocrinology and Reproduction Research Branch, National Institute of Child Health and Human Development, National Institutes of Health, Building 49, Room 6A-36, 49 Convent Drive, Bethesda, Maryland 20892-4510. E-mail: stankos{at}helix.nih.gov

Calcium can serve not only as an intracellular messenger, but also as an extracellular messenger controlling the gating properties of plasma membrane channels and acting as an agonist for G protein-coupled Ca²⁺-sensing receptors. Here we studied the potential extracellular messenger functions of this ion in anterior pituitary cells. Depletion and repletion of the extracellular Ca²⁺ concentration ([Ca²⁺]_e) induced transient elevations in the intracellular Ca²⁺ concentration ([Ca²⁺]_i), and elevations in [Ca²⁺]_e above physiological levels decreased [Ca²⁺]_i in somatotrophs and lactotrophs, but not in gonadotrophs. The amplitudes and duration of [Ca²⁺]_i responses depended on the [Ca²⁺]_e and its rate of change, which resulted exclusively from modulation of spontaneous voltage-gated Ca²⁺ influx. Changes in [Ca²⁺]_e also affected GH and PRL secretion. The PRL secretory profiles paralleled the [Ca²⁺]_i profiles in lactotrophs, whereas GH secretion was also stimulated by [Ca²⁺]_e independently of the status of voltage-gated Ca²⁺ influx. [Ca²⁺]_e modulated GH secretion in a dose-dependent manner, with EC₅₀ values of 0.75 and 2.25 mM and minimum secretion at about 1.5 mM. In a parallel experiment, cAMP accumulation progressively increased with elevation of [Ca²⁺]_e, whereas inositol phosphate levels were not affected. These results indicate the cell type-specific role of [Ca²⁺]_e in the control of Ca²⁺ signaling and secretion.

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