The electrophysiological and metabolic responses to insulin of skeletal muscles from control and potassium-depleted rats were compared. Membrane potentials, action potentials, contraction parameters as well as oxygen uptake were measured in diaphragm strips or intact extremity muscles from the two groups, and similar measurements were made in vivo. The muscles were examined in solutions with normal potassium concentration [K]o , reduced [K]o, and in normal [K]o and in normal [K]o with ouabain, in each case before and after insulin, 400 mU/ml. In normal solution, the depleted muscle contractions were weaker and slower than control. The depleted muscles, already having low potassium conductance, are paralysed by the further reduction of potassium conductance after insulin. Hyperpolarising effects of insulin-induced Na/K pumping are offset in the depleted muscles with a high sodium conductance and low [K]o. Respiration is about normal at rest in depleted muscles, despite increased [Na]i, suggesting that the sodium is sequestered. After insulin, reduction of [K]o, or ouabain plus insulin, the depleted fibres take up more O2 than controls. In the presence of ouabain, this respiratory stimulation is believed to represent response to Ca++ influx. The K-depleted rat does not seem to be an entirely satisfactory model of the human disease hypokalaemic periodic paralysis.
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