Helical strips of rat tail artery were observed to relax in response to potassium after contraction induced by 10<sup>–7</sup> 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<sup>+</sup>-K<sup>+</sup> ATPase. This assumption seemed justified because the observed amplitude of potassium-induced relaxation paralleled known effects of the following variables on Na<sup>+</sup>-K<sup>+</sup> 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<sup>+</sup>-K<sup>+</sup> 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<sup>+</sup>-K<sup>+</sup> ATPase activity in vascular smooth muscle.