Effects of dipyridamole on the smooth muscle of the guinea-pig's taenia coli were studied using the single and double sucrose gap method. Dipyridamole (10(-5) M) affected neither the non-adrenergic inhibitory junction potential, elicited by field stimulation, nor the membrane hyperpolarization induced with ATP applied exogenously, but did potentiate the accompanying relaxations. The muscle spike activity was reduced by dipyridamole without affecting the membrane potential or the membrane resistance. Carbachol induced a depolarization of the muscle cell membrane and thus a contraction of the muscle. Dipyridamole did not modify the membrane potential change produced by carbachol but decreased the size and time course of the contraction. From these results it is concluded that dipyridamole does not potentiate non-adrenergic relaxations by interfering with the neuromuscular transmission, which has been assumed to be purinergic.