Mechanism of regulation of amylase release by .ALPHA.- and .BETA.-adrenergic agonists in rat parotid tissue.

Publisher Website
Google Scholar
Abstract
The effect of forskolin and isobutyl-methylxanthine on amylase release and cAMP accumulation by .alpha.- and .beta.-adrenergic agonists was studied in rat parotid slices. A small increase in cAMP by .beta.-adrenergic agonists was sufficient for maximum stimulation of amylase release, but a similar increase in cAMP by forskolin did not stimulate the maximum amount of amylase release. The amount of amylase release and cAMP changed in parallel when lower doses of isobutyl-methylxanthine were used, but higher doses of isobutyl-methylxanthine further increased cAMP without causing a significant increase in amylase release. Amylase release stimulated to its maximum by isobutyl-methylxanthine was much lower than that by isoproterenol. cAMP evidently, is not the only chemical correlate for the activation of amylase release by .beta.-adrenergic agonists. The effect of phenylephrine and methoxamine on amylase release was augmented by either forskolin or isobutyl-methylxanthine, but the effect of methacholine was not. Phenylephrine increased the cAMP concentration under the same conditions, but methoxamine did not. The inhibition of the effect of phenylephrine plus forskolin on cAMP accumulation by propranolol was almost complete and stereospecific, but the inhibition of their effects on amylase release was incomplete and not stereospecific. Synergism of amylase release was observed in the effect between methoxamine and dibutyryl cAMP. The augmentation of the effect of .alpha.-adrenergic agonists on amylase release by forskolin or isobutyl-methylxanthine cannot be explained only on changes in cAMP. Some other factor in collaboration with cAMP may participate in the regulation of amylase release by .alpha.-adrenergic agonists.