Secretion of calcitonin in hypocalcemic states in man.

The control of calcitonin secretion in humans has been studied extensively only in patients with medullary thyroid carcinoma since the peripheral concentration of the hormone in normal subjects is too low for accurate measurement by existing assay procedures. However, we have recently found that the concentrations of calcitonin in the peripheral plasma of hypocalcemic subjects during provocative tests of hormone secretion were high enough to be measured by radioimmunoassay. Accordingly, the effect of calcium and pentagastrin infusions on plasma calcitonin was studied in nine patients with pseudohypoparathyroidism, seven patients with idiopathic hypoparathyroidism, and six patients with hypocalcemia not due to parathyroid disease. The infusion of calcium in these hypocalcemic subjects resulted in increases in plasma calcitonin to levels that could be readily detected by our radioimmunoassay. Pentagastrin infusion also caused an increase of plasma calcitonin in some subjects, but calcium was approximately 10 times more effective than gastrin in its stimulatory effect on hormone secretion. These results demonstrate that in humans as well as other mammals the secretion of calcitonin by parafollicular cells that are not involved by medullary thyroid carcinoma is directly related to plasma calcium and that gastrin can also stimulate hormone secretion. The results are consistent with the thesis that the secretion of calcitonin by normal human subjects does occur but at peripheral concentrations of the hormone below the detection limits of most existing immunoassays; hypocalcemia leads to increased stores of hormone that can be related by the appropriate stimuli.