Thyrotropin-induced acceleration of calcium efflux from mouse thyroid: evidence for inhibition by excess iodide

We investigated the effect of TSH on calcium transport in mouse thyroid, as well as the influence of iodide thereupon. Thyroid lobes were incubated in Krebs-Ringer bicarbonate buffer containing [45Ca2+] and the time-dependent uptake of [45Ca2+] by the lobes was observed. In the presence of 0.5 mU/ml TSH, the uptake of [45Ca2+] was significantly depressed at early phases of incubation (from 20 to 40 min). Similarly, (Bu)2cAMP (DBC) depressed the [45Ca2+] uptake. The efflux of calcium was also studied by using thyroid lobes preloaded with [45Ca2+]. In the presence of 0.5 mU/ml TSH, [45Ca2+] release from the lobes was doubled in comparison with the control lobes incubated without TSH. DBC similarly accelerated [45Ca2+] release from the lobes. The acute administration of excess iodide to mice fed a low iodine diet inhibits the TSH-induced adenylate cyclase activation in thyroids. The acceleration of calcium efflux induced by TSH was completely abolished by the acute administration of excess iodide in thyroids obtained from animals fed a low iodine diet. Similarly, DBC-induced acceleration of calcium efflux was inhibited by pretreatment with excess iodide. However, the inhibitory effect of iodide on TSH- or DBC-induced acceleration of calcium efflux was not observed in thyroids obtained from mice fed a regular diet. Inhibition of TSH-induced acceleration of calcium efflux by iodide was diminished by treatment of mice with methimazole before iodide. These results suggest that 1) TSH accelerates calcium efflux from the thyroid as a result of accumulation of cAMP in the thyroid, and that 2) iodide inhibits calcium efflux by inhibition of TSH-induced adenylate cyclase activation and by inhibition of the mechanism(s) which is (are) activated by cAMP.