Canine femoral arteries responded to acetylcholine with relaxations; these were abolished in potassium free solution, restored by potassium or rubidium but not by cesium or amonium. Potassium and rubidium were equipotent in inducing ouabain-sensitive relaxation, while amonium and cesium were less potent. The results (1) confirm that sodium-potassium exchanges are indirectly involved in cholinergic relaxation of arterial smooth muscle and (2) suggest that membrane hyperpolarisation resulting from increased electrogenic sodium transport does not affect the inhibitory response to the cholinergic transmitter.