Helical strips of rat tail artery were observed to relax in response to potassium after contraction induced by 10–7 g/ml norepinephrine in potassium-free solution. After several minutes of relaxation, the strips showed an abrupt redevelopment of tension. The amplitude of the potassium-induced relaxation was employed as an index of the activity of the electrogenic sodium-potassium pump and hence of the Na+-K+ ATPase. This assumption seemed justified because the observed amplitude of potassium-induced relaxation paralleled known effects of the following variables on Na+-K+ ATPase: (1) intracellular sodium concentration; (2) ouabain administration; (3) magnesium; (4) temperature, and (5) potassium concentration. The relaxation that occurred in response to potassium is suggested to be due to an enhanced Na+-K+ ATPase resulting in increased electrogenic transport of sodium and potassium and, consequently, hyperpolarization. We propose that potassium-induced relaxation of rat tail artery may be used as a functional indicator of Na+-K+ ATPase activity in vascular smooth muscle.