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Research Article Free access | 10.1172/JCI107499

Skeletal Muscle Resting Membrane Potential in Potassium Deficiency

Gordon L. Bilbrey, Luis Herbin, Norman W. Carter, and James P. Knochel

Department of Medicine, The University of Texas Southwestern Medical School, Dallas, Texas 75235

Department of Medicine, Veterans Administration Hospital, Dallas, Texas 75216

Find articles by Bilbrey, G. in: JCI | PubMed | Google Scholar

Department of Medicine, The University of Texas Southwestern Medical School, Dallas, Texas 75235

Department of Medicine, Veterans Administration Hospital, Dallas, Texas 75216

Find articles by Herbin, L. in: JCI | PubMed | Google Scholar

Department of Medicine, The University of Texas Southwestern Medical School, Dallas, Texas 75235

Department of Medicine, Veterans Administration Hospital, Dallas, Texas 75216

Find articles by Carter, N. in: JCI | PubMed | Google Scholar

Department of Medicine, The University of Texas Southwestern Medical School, Dallas, Texas 75235

Department of Medicine, Veterans Administration Hospital, Dallas, Texas 75216

Find articles by Knochel, J. in: JCI | PubMed | Google Scholar

Published December 1, 1973 - More info

Published in Volume 52, Issue 12 on December 1, 1973
J Clin Invest. 1973;52(12):3011–3018. https://doi.org/10.1172/JCI107499.
© 1973 The American Society for Clinical Investigation
Published December 1, 1973 - Version history
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Abstract

The resting transmembrane potential of skeletal muscle (Em) is thought to be a function of the ratio of intracellular to extracellular potassium concentration ([Ki]/[Ko]). In potassium deficiency, the fall of [Ki] is proportionately less than the fall of [Ko], thus theoretically predicting a rise of Em. To examine this theory and to characterize Em in kaliopenic myopathy, muscle composition and Em were measured during moderate (n = 5) and severe (n = 11) K deficiency in the dog and compared with measurements in the severely K-deficient rat (n = 10). Mean measured Em rose during moderate K deficiency in four of five dogs (-85.4 to -94.6 mV) and during severe K deficiency in the rat (-89.1 to -94.9 mV). Both values closely approximated the increase in Em predicted by the Goldman equation. In contrast, during severe K deficiency in the dog, a significant decline (P < 0.001) of mean Em to -55 mV was observed.

Since skeletal myopathy and paralysis do not occur in the rat as a consequence of K deficiency, the observation that Em falls as paralysis occurs in the unexercised dog suggests that alteration of muscle membrane function may play a role in kaliopenic myopathy. Such an event could explain the ease with which frank muscle necrosis may be induced by exercise in the K-deficient dog.

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