Abstract
Antiorthostatic hindlimb suspension reduces resting membrane potential of rat fast and slow muscles within 7 days. Changes in Na+/K+ pump activity and shifts of the equilibrium potential for chloride ions are the main mechanism of the changes in the resting potential of muscle fibers. The latter is presumably associated with increased intracellular ion current due to activation of the second active Na+, K+, 2Cl- symport. Reduction of the membrane potential is related to muscle denervation. However, membrane depolarization of muscle fibers during antiorthostatic suspension cannot be explained solely by changes in the mechanisms of neurotrophic control from motor neurons.
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