Amylase release from parotid glands of hypothyroid rats. I. Altered responsiveness to adrenergic agents

Effects of adrenergic agents on alpha- and beta-adrenergic receptors of parotid glands from hypothyroid rats were compared with those of euthyroid rats. The sensitivity for amylase release from parotid slices to adrenergic agents did not change even in hypothyroid status because ED50 values for amylase release in both groups were approx. the same: 7 x 10(-8) M for isoproterenol, 4-6 x 10(-6) M for phenylephrine and 10(-5) M for methoxamine. However, the responsiveness of the tissue to those agents which was determined as the maximal amylase release was significantly higher in hypothyroid status than in the euthyroid status. The maximal increases in amylase release in euthyroid and hypothyroid rats were approx. 7.4% and 10.0% of the total in isoproterenol, 3.9% and 7.4% of the total in phenylephrine and 1.3% and 2.7% of the total in methoxamine, respectively. The effect of dibutyryl cyclic AMP mimicked that of isoproterenol, and the responsiveness of the tissue in this case was much higher in the hypothyroid rats than in the euthyroid rats. Furthermore, 10 mM tolbutamide, which completely inhibited the activity of cyclic AMP-dependent protein kinase, blocked isoproterenol-induced amylase release by 66.5% in euthyroid rats, against only 36.3% in hypothyroid rats. These results strongly suggest that the regulation mediated through beta-adrenergic receptors plays a major role in amylase release from rat parotid glands even under hypothyroid status, and the step following cyclic AMP synthesis might, at least in some way, be involved in this regulation.