1. The membrane potential (Vm) of fibres of the extensor digitorum longus (EDL) of the mouse, measured at 35 degrees C and with extracellular potassium concentration (K+o) 5.7 mM, was Vm = ‐76 mV. 2. Lowering K+o below 1 mM could lead to either a hyperpolarizing or a depolarizing response. When Vm was lower than ‐75.5 mV in the control medium, a reduction of K+o to 0.76 mM led to a hyperpolarization of Vm (‐95.0 +/‐ 0.7 mV, n = 40); otherwise a depolarization occurred (Vm = ‐47.2 +/‐ 1.1 mV, n = 21). 3. The difference in Vm responses did not correlate consistently with functional differences in cell types, as cells that originally hyperpolarized, could later depolarize. 4. The observed phenomena could be explained if the properties of the anomalous rectifier, AR (or inward‐going rectifier), are considered to be similar to those observed in cardiac cells. 5. Apparently caesium acted as a competitive inhibitor; when the inhibition was strong enough the non‐linear properties of the AR regeneratively amplified the depolarization to the full‐blown depolarized state (Vm = ‐46.7 +/‐ 1.3 mV, n = 15). 6. Ouabain (10(‐4) M) reduced Vm (to ‐45 +/‐ 3 mV, n = 5) and reduced dramatically the selectivity of the cell membrane for potassium over sodium. These effects could be reversed readily by washing out the ouabain. 7. Adrenaline (2 microM) added to the medium hyperpolarized Vm (delta Vm = ‐4.6 +/‐ 1.4 mV, n = 9) and increased the changes induced by lowered K+o (from ‐14.3 +/‐ 0.5 mV, n = 5 to ‐18.0 +/‐ 0.8 mV, n = 9); the cells that originally depolarized when K+o was lowered could hyperpolarize after adrenaline addition.