The sensitivity of the rat submaxillary gland was examined 3-4 weeks after either parasympathetic decentralization or sympathetic decentralization or denervation. The threshold doses for secretion of saliva of parasympathomimetic (methacholine) and sympathomimetic (noradrenaline, adrenaline, phenylephrine and isoprenaline) drugs were estimated and the amount of saliva secreted in response to supraliminal doses of these drugs was measured. Each type of operation caused the development of a supersensitivity that involved all three types of receptors, i.e. muscarinic cholinoceptors, alpha-adrenoceptors and beta-adrenoceptors. Following parasympathetic decentralization the sensitization was predominantly mediated via alpha-adrenoceptors, and also via cholinoceptors. Following sympathetic decentralization or denervation the postjunctional sensitization was predominantly mediated via beta-adrenoceptors; most of the supersensitivity to noradrenaline, adrenaline and phenylephrine found after sympathetic denervation was of the prejunctional type. An increase in receptor density and an intracellular arrangement where the response of cholinoceptors and alpha-adrenoceptors is mediated via one pathway and the response of beta-adrenoceptors via another are suggested as factors that may be of importance for the development of the postjunctional supersensitivity. The present study shows that the traffic of secretory impulses in the sympathetic nerve is of importance for the level of sensitivity of the secretory cells. Since postjunctional supersensitivity following sympathetic denervation did not exceed that following sympathetic decentralization it is suggested that under normal conditions a continuous release of noradrenaline from the nerve endings is of little importance for the level of sensitivity.