In denervated guinea-pig diaphragm the depolarization produced by decamethonium (100 microM) was followed by an initial phase of recovery, and then by a slow restoration of membrane potential in the presence of the drug, with hyperpolarization. Membrane potentials were measured by repeated insertions. The slow phase of spontaneous recovery was not found in the absence of potassium or in the presence of ouabain (100 microM). 2. With 1 microM-decamethonium the net loss of potassium from denervated muscle was 17% by wet weight in 20 min as compared with controls, which represents a loss of over 30 mM in internal concentration. Similar results were obtained with 100 microM-decamethonium. Spontaneous recovery of potassium occurred in the succeeding 2 h in the presence of 1 microM and 100 microM-decamethonium. With 5 nM-decamethonium muscles exposed for 20 min had a potassium content which was not reduced as compared with controls. 3. In rat diaphragm decamethonium (100 microM) also produced depolarization and slow spontaneous recovery which was not seen in the absence of potassium or the presence of ouabain. With 3 mM-decamethonium spontaneous recovery of potential was complete in 5 min. 4. Change from 5 mM-potassium to potassium-free solution produced consistent hyperpolarization in denervated guinea-pig diaphragm. In rat diaphragm at 38 degrees C the results were variable, with some fibres showing hyperpolarization while others showed depolarization.
