1. Sodium fluoride (10−2 M), 2,4-dinitrophenol (10−4 M), and iodoacetate (10−4 M) caused a slight decrease in potassium uptake by the uterus and fluoride and dinitrophenol caused a larger and immediate increase in efflux, resulting in a net loss of potassium. There was apparently a delayed increase in efflux caused by iodoacetate. The effects of inhibitors on efflux were not prevented by the absence of external potassium. The effects of fluoride suggested that it produced inhomogeneity in uterine potassium and analysis of the longitudinal muscle layer separately from the remainder of the uterus suggested that efflux was speeded more in myometrium than in endometrium. This was attributed to the prolonged contracture induced by fluoride. The depolarization required to explain the increases in efflux produced by fluoride and DNP was sufficient to explain the decreases in influx. It was postulated that these inhibitors act by causing depolarization which might be the result of inhibition of an electrogenic sodium pump. Iodoacetate 10−3 M caused a 50% reduction in potassium influx and probably a large immediate increase in efflux, but no evidence was obtained that this concentration caused contraction.2. Ouabain in concentrations as high as 10−5 M had only minor effects on potassium inward and outward movements and on reaccumulation of potassium and extrusion of sodium during recovery from exposure to the cold. The resistance of rat uteri to cardiac glycosides derives either from insensitivity in rat tissues or from a unique feature of sodium transport in the rat uterus.3. When KCl was added to the Ringer fluid, there was no net gain of cellular potassium relative to dry weight. Osmotic balance was achieved mainly by water loss from cells, but uncertainty as to the extracellular fluid volume prevented a definite conclusion. When KCl was omitted from the Ringer fluid, there was a 50% decrease in efflux, suggesting that a part of the potassium movement was "exchange diffusion". The assumption of exchange diffusion also would aid in explaining the observed flux ratio near unity in view of the values reported for membrane potentials of uterine cells. Owing to the lack of data regarding intracellular activity of potassium and the incompleteness of data on membrane potentials of uterine cells, it was not possible to prove whether active influx of potassium was present or absent in addition to that entering passively either by free diffusion or exchang diffusion.