Effects of carbachol on isoprenaline evoked amylase release from the rabbit parotid gland in vitro.

Amylase secretion from dispersed lobules of the parotid gland of the rabbit was studied in response to isoprenaline (10(-8)-10(-5) M) and to carbachol (10(-8)-10(-5) M). The effects of each agent were investigated along and in combination at certain concentrations. Isoprenaline produced a dose-related amylase secretion with an average maximum of 688 units/100 mg, at 10(-5) M. The amylase secretion produced by submaximal concentrations of isoprenaline could be further increased by carbachol, already in low concentrations (10(-8)-10(-7) M), that were subthreshold for amylase secretion. This potentiating effect was seen not only as a larger secretion but also as a greater depletion of amylase from the tissue. In contrast to what is known from experiments in vivo, carbachol in a high concentration (10(-5) M), by activating muscarinic receptors only, released amylase to the same extent as that released by isoprenaline. This concentration of carbachol regularly decreased the amylase secretion evoked by isoprenaline, and may be regarded as unphysiologically high. The increase in isoprenaline evoked amylase secretion, brought about by carbachol in lower concentrations, may be due to an improved transport of amylase, because of secretion of fluid, but could also be caused by augmentation of the beta-adrenoceptor mediated effects.