α1-adrenergic regulation of thyrotropin-stimulated release of 3, 5, 3’ -triiodothyronine and thyroxine from perifused mouse thyroid

Abstract

The effect of methoxamine, a specific alpha 1-adrenergic agonist, on the release of T3, T4 and cAMP from perifused mouse thyroid was studied to clarify the role of the alpha 1-adrenergic receptor in the regulation of thyroid hormone secretion. TSH-stimulated T3 and T4 release was inhibited significantly by methoxamine. With regard to cAMP release, methoxamine inhibited TSH-stimulated cAMP release in the presence of 4-(3-butoxy-4-methoxybenzyl)-2-imidazolidinone but did not inhibit TSH-stimulated cAMP release in the presence of 3-isobutyl-1-methylxanthine. Methoxamine did significantly suppress TSH-stimulated release of T3 and T4 in the presence of each phosphodiesterase inhibitor. Depletion of Ca2+ in the perifusion buffer abolished completely the inhibitory effect of methoxamine on TSH-stimulated T3 and T4 release. The present study suggests that activation of the alpha 1-adrenergic receptor inhibits TSH-stimulated T3 and T4 secretion through a Ca(2+)-dependent mechanism in the mouse thyroid gland.

The inhibitory effect of noradrenaline on thyrotrophin-stimulated 3,5,3′-tri-iodothyronine and thyroxine release is mediated through a Ca2+-dependent process in the thyroid gland of the mouse

“…Based upon electron microscopic examination of rat thyroid glands perifused with TSH and iono¬ phore A23187, we concluded that this suppression may be the result of the inhibition of colloid reabsorp¬ tion . We have also shown in the mouse thyroid that methoxamine, a specific ar adrenergic agonist, inhibits TSH-stimulated T3 and T4 release through an increase in cytosolic Ca2+ (Oda et al 1991). These observations support the hypothesis that noradrenaline may inhibit thyroid hormone secretion through a Ca2+-dependent process.…”

Neural correlates of free T3 alteration after catecholamine depletion in subjects with remitted major depressive disorder and in controls

“…Consistent with our a priori hypothesis, serum FT3 and FT4 levels were less suppressed under AMPT than they were under placebo treatment in the whole sample. Previous research has suggested that catecholamines block the TSH-induced stimulation of thyroid cells in vitro (Maayan 1990;Oda et al 1991). Thus, the relative elevations in FT3 and FT4 levels observed might be attributable to decreased catecholaminergic neurotransmission.…”

“…Because of the conflicting results regarding the relationship between thyroid hormones and depression (Joffe 1993), we based our hypotheses on relatively solid endocrinological data linking catecholamines to thyroid hormones. Since dopaminergic transmission inhibits TSH secretion (Kaptein et al 1980), and catecholamines block the TSH-induced stimulation of thyroid cells in vitro (Maayan 1990;Oda et al 1991), we hypothesized that catecholamine depletion results in higher serum TSH and thyroid hormone levels compared with placebo treatment. In addition, we expected that even small effects of catecholamine depletion on thyroid hormones, within the euthyroid state, would suffice to induce clinically relevant mood effects since the brain seems to be sensitive to small changes in thyroid hormone Homan et al 5 levels (Joffe 1993;Meyer and Hesch 1983;Schueler et al 1990;Yamada and Wilber 1990).…”