IT has been proposed that the physiological action of calcitonin is to prevent or diminish postprandial hypercalcaemia1. This is accomplished by inhibition of bone resorption2, of the tubular reabsorption of calcium3, and of the intestinal absorption of calcium4. Secretion or release of the hormone by parafollicular cells of the thyroid gland is mediated by calcium5-7 and by gastrointestinal hormones including gastrin and pancreozymin8,9. Secretion is apparently influenced by the adenylate cyclase system 7,10 and hormonal regulation presumably is mediated by cyclic adenosine 3′, 5′-monophosphate (cyclic AMP).
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