Role of voltage-dependent calcium channels in secretion of calcitonin from human medullary thyroid carcinoma cells

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Abstract
Extracellular calcium concentration is an important regulator of calcitonin secretion. We used primary cell cultures of human medullary thyroid carcinoma to study the role of voltage dependent calcium channels for stimulus secretion coupling. Increasing extracellular calcium concentration (1.6–5.0 mM) in the medium caused a dose dependent release of calcitonin. The calcium channel activator BAY K 8644, a dihydropyridine, stimulated calcitonin secretion in a dose dependent manner (10−7−10−5 M). This effect was completely inhibited by equimolar concentrations of the calcium channel blocker nifedipine and abolished in the absence of extracellular calcium. Similarly, nifedipine suppressed the stimulatory action of extracellular calcium. The effects of calcium and BAY K 8644 with and without nifedipine suggest that calcium influx via voltage dependent calcium channels plays an important role in calcitonin secretion. The primary cell culture of human medullary thyroid carcinoma is a good model for the study of stimulus secretion coupling.

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