Abstract

The effects of pharmacological doses of calcium ionophores, calcitonin and 1,25 (OH2)D3, and of the calmodulin inhibitor, trifluoperazine, on thyrotropin secretion at rest and TRH stimulated secretion were investigated as well as their mutual interactions in five groups of clinically healthy volunteers. The thyrotropic secretory response to TRH was inhibited by a single intravenous dose of 50 U synthetic salmon calcitonin or trifluoperazine administered by mouth seven days prior to the TRH test, 6-12 mg/day, and stimulated by 1,25(OH)2D3 administered by mouth four days before the TRH test -3 micrograms/day. The stimulating action of 1,25(OH)2D3 was abolished by calcitonin, administered by the intravenous route - 50 U - closely before the TRH test but not by the concomitant administration of trifluoperazine. The author expressed the hypothesis, that calcitonin and 1,25(OH)2D3 but not trifluoperazine and 1,25(OH)2D3 are mutual antagonists which act at the same subcellular level of the thyrotropic cell and that synthesis and activation of calmodulin is not the trigger of thyrotropic secretion after stimulation with 1,25(OH)2D3. An altered thyrotropin secretion must be foreseen during the therapeutic administration of the investigated calciotropic substances, the mutual interactions of which could be used in practice.

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