Thyrotrophin increases the α1b-adrenergic receptors in rat thyroid gland in vivo

Abstract

Using chlorethylclonidine (CEC), an alpha 1b-adrenergic receptor-selective antagonist, we characterized alpha 1-adrenoceptor subtypes in rat thyroid gland, and investigated the effect of methimazole (MMI)-induced high TSH levels on alpha 1 receptor subtypes and noradrenaline-induced iodide organification. The density of thyroid alpha 1-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 mumol/l) caused an 83% decrease in specific 2-[beta-(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 alpha 1 receptors (alpha 1a) was similar in MMI-treated and control rats, so MMI was shown to increase CEC-sensitive alpha 1 receptors (alpha 1b). 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 mumol CEC/l 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 alpha 1a and alpha 1b receptors, both of which mediate noradrenaline-induced iodide organification, and also that TSH enhances noradrenaline-induced iodide organification by increasing alpha 1b receptor density.