Stimulation of alpha-amylase release and cyclic AMP accumulation by catecholamine in rat parotid slices in vitro.

Abstract

The role of cyclic AMP in α-amylase release by catecholamines was studied in rat parotid slices. The order of potency required for catecholamines to induce α-amylase release as well as cyclic AMP accumulation was as follows: isoproterenol>norepinephrine=epinephrine>> phenylephrine. At the lowest concentration tested, all of the catecholamines stimulated α-α-mylase release without causing a detectable accumulation of cyclic AMP. High doses of phenylephrine and other derivatives of catecholamines such as salbutamol and soterenol stimulated α-amylase release, but they did not cause accumulation of cyclic AMP and their maximum effects on α-amylase release were significantly lesser than those of norepinephrine. High concentrations of these derivatives decreased the effect of norepinephrine on α-amylase release, which may be attributed to be the cause of this smaller maximum effect. The stimulation of cyclic AMP accumulation by norepinephrine was much more sensitive to inhibition by β-adrenergic antagonists than was the stimulation of α-amylase release by norepinephrine. The effect of norepinephrine on cyclic AMP accumulation was potentiated by isobutylmethylxanthine, which correlated with the degree of inhibition of phosphodiesterase. The effect of low doses of norepinephrine on α-amylase release was increased by isobutyl-methylxanthine, but there was no such effect when either high doses of norepinephrine or dibutyryl cyclic AMP was used. The stimulation of α-amylase release by 1 μm norepinephrine was much greater than that by 0.2 μM norepinephrine plus 0.5 mm isobutylmethylxanthine, while the reverse was took place in cyclic AMP accumulation. Thus, there was a marked dissociation of cyclic AMP accumulation and α-amylase release. The bearing of these results on the role of cyclic AMP in α-amylase release was discussed.