Noradrenergic and dopaminergic modulation of thyrotropin secretion in the rat
Noradrenergic and dopaminergic regulation of thyrotropin (TSH) secretion was investigated in adult male Wistar rats. TSH secretion displayed a circadian variation with peak serum TSH levels at 10.00 h. The α2-adrenoceptor agonist, clonidine (250 μg/kg, i.p.), was found to cause an enhancement of serum TSH levels at 10.00 h (160 ± 10% of control values, P < 0.001) which was antagonized by prior administration of the α2-adrenoceptor antagonist, yohimbine (3 mg/kg, i.p.). The α-adrenoceptor antagonist phentolamine caused a significant decrease in serum TSH levels at 10.00 h (62 ± 15% of control values, P < 0.05) at a dosage of 2 mg/kg, i.p. The α1-adrenoceptor agonist, phenylephrine (0.2 or 2 mg/kg, i.p.), was without effect as were the dopaminergic receptor agonist, apomorphine (1 or 5 mg/kg, i.p.), and the antagonist, sulpiride (20 mg/kg, i.p.). The β-adrenoceptor agonist, isoproterenol (1 mg/kg, i.p.) was found to cause a decrease in serum TSH levels at 10.00 h (70 ± 16% of control levels, P < 0.01), which was completely antagonized by prior administration of the β-adrenoceptor antagonist, propranolol (10 mg/kg, i.p.).TSH-releasing hormone (TRH, 5 μg/kg, i.v.) caused a significant stimulation of TSH secretion (470 ± 63% of basal levels, P < 0.001), which was not affected by prior treatment of the rats with yohimbine (0.1 mg/kg, i.p.), phentolamine (2 mg/kg, i.p.), propranolol (10 mg/kg, i.p.) or sulpiride (20 mg/kg, i.p.). There was, however, a tendency towards a decrease in the TRH-stimulated release of TSH in rats pretreated with phentolamine or propranolol. The results of this study clearly demonstrate the existence of stimulatory α2-adrenoceptors as well as inhibitory β-adrenoceptors which modulate TSH secretion in vivo and which can be used to test noradrenergic receptor responsiveness under different pharmacological conditions.