Using chlorethylclonidine (CEC), an αlb-adrenergic receptor-selective antagonist, we characterized α1-adrenoceptor subtypes in rat thyroid gland, and investigated the effect of methimazole (MMI)-induced high TSH levels on α1 receptor subtypes and noradrenaline-induced iodide organification. The density of thyroid α1-adrenergic receptors was increased about sixfold in rats treated with MMI for 3 weeks compared with controls. Pretreatment of thyroid membrane preparations with CEC (10 μmol/l) caused an 83% decrease in specific 2-[β-(hydroxy-3-[125I]iodophenyl) ethylaminomethyl]tetralone binding sites in MMI-treated rats, but only a 43% decrease in control rats. The density of CEC-insensitive α1 receptors (α1a) was similar in MMI-treated and control rats, so MMI was shown to increase CEC-sensitive α1 receptors (α1b).
Noradrenaline-stimulated iodide organification was threefold greater in MMI-treated rats than in control rats when values were expressed as a per cent increase over basal levels. Pretreatment of thyroid lobes with 10 μmol CEC/1 for 30 min caused a 66% decrease in maximal noradrenaline-induced iodide organification in MMI-treated rats, but a significantly lower decrease (49%) in control rats.
These results suggest that the rat thyroid gland contains both α1a and α1b receptors, both of which mediate noradrenaline-induced iodide organification, and also that TSH enhances noradrenaline-induced iodide organification by increasing α1b receptor density.
Journal of Endocrinology (1990) 126, 317–322
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