Abstract-Oxygen uptake and amylase output in rat submandibular gland slices were measured by utilizing adrer,_rgic agonists. Adrenaline, noradrenaline and isoproterenol significantly stimulated the oxygen uptake and amylase output. In the presence of propranolol or phenoxybenzamine, adrenaline-stimulated oxygen uptake was obviously blocked. Adrenaline-stimulated amylase output was inhibited by propranolol, but was not inhibited by phenoxybenzamine. The increase in oxygen uptake by nor adrenaline was blocked by phenoxybenzamine, but not by propranolol.Isopro terenol-stimulated oxygen uptake and amylase output were strongly inhibited by propranolol.The oxygen uptake due to isoproterenol was little affected by phenoxy benzamine. These results suggest that the increase in oxygen uptake seen with adrenergic agonists is mediated by both a and n-receptors, and that the amylase output is evoked through the stimulation of j3-receptors.The term "stimulus-secretion coupling" was originally coined by Douglas and Rubin (1, 2) to describe the sequence of events initiated by acetyicholine (ACh) stimulation of adrenal chromaffin cells and leading to the secretion of catecholamines by exocytosis.They apparently had in mind the close similarity to the phenomenon of "excitation contraction coupling" in muscle (namely, the key role of calcium in mediating both secretion and contraction and the parallel set of electrical and ionic events at the plasma membrane in response to ACh). We previously reported that the oxygen uptake in dog submandibular gland slices was stimulated by addition of ACh (10-4-5 x 10-3 M) and K+ (14.25-57 mM) (3). Both K+ and ACh-stimulated oxygen uptake was inhibited by Ca2+ omission from the incubation medium, and the reversibility of the effects of K+ and ACh was recognized by the addition of 5 mM Ca2+. These results suggested that Caz+ plays an important role in the oxygen uptake response to K+ and ACh of the submandibular gland slices.Pieces or slices of rat parotid gland, incubated in vitro, respond to adrenaline and carbachol by increasing a-amylase output and oxygen uptake (4, 10). Adrenaline activates amylase secretion through Q-receptors and K+ release through a-receptors (5, 6). Phenyl ephrine increases amylase output through the stimulation of both a and Q-receptors (4, 12).The increasing concentration of cyclic AMP in the acinar cells is involved in the increase of amylase output by adrenaline and phenylephrine. Lindsay et al. (7) reported that a amylase secretion from rat parotid tissue in vitro was neither critically dependent on nor closely related to any of the accompanying alterations in tissue metabolism (glucose and
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