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

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

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