Mechanisms of the exogenic acetylcholine (ACh) effect on ionic currents of nerve endings (NE) were investigated by extracellular recording of NE at the cutaneous pectoris muscle of frog. It was found that ACh in concentrations 0.1-0.6 mmol/l increased the third phase of the nerve ending response, while in concentrations 0.7-2.0 mmol/l-decreased it. Tubocurarine and atropine did not alter the ACh effect. It has been also revealed that growth of the third phase of NE response, induced by ACh, occurs in the presence of calcium channel blockers and disappears under the influence of 4-aminopyridine and tetraethylammonium. In calcium-free solution or when the calcium current is blocked the suppressive effect of ACh disappears. The mechanisms of exogenic and endogenic ACh effects on the potential-sensitive and calcium-activated potassium NE currents are discussed.