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

Publisher Website
Google Scholar
Abstract
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 approximately the same: 7 .times. 10-8 M for isoproterenol, 4-6 .times. 10-6 M for phenylephrine and 10-5 M for methoxamine. 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 .apprx. 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 cAMP 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. Ten mM tolbutamide, which completely inhibited the activity of cAMP-dependent protein kinase, blocked isoproterenol-induced amylase release by 66.5% in euthyroid rats, against only 36.3% in hypothyroid rats. The regulation mediated through .beta.-adrenergic receptors apparently plays a major role in amylase release from rat parotid glands even under hypothyroid status, and the step following cAMP synthesis might, at least in some way, be involved in this regulation.