K‐depletion induced by K‐deficient fodder led to hypokalemia, decreased K‐content and increased Na‐content in skeletal muscle of rats. The heart showed similar, although more modest changes, whereas brain, erythrocytes and liver maintained virtually constant Na–K‐contents. K‐depletion decreased total binding capacity for 3H‐ouabain by up to 76%, an effect which could be demonstrated both in vitro and in vivo. Following 3 weeks of K‐depletion, the apparent KD for 3H‐ouabain binding to rat soleus was 1.3times10‐7 M as compared to 2.4times10‐7 M in controls. Also in mice and guinea pigs, K‐depletion induced a selective loss of K from muscle and decreased 3H‐ouabain binding capacity. K‐depletion induced by diuretics or fluorohydrocortisone gave similar effects. The effects of K‐depletion on 3H‐ouabain binding capacity were confirmed by measurements of 3‐O‐methylfluorescein phosphatase activity, an enzyme activity which is closely correlated to the Na–K–ATPase activity. Following readministration of K, the K‐contents of plasma and muscle reached control levels in 24 hours, but 3H‐ouabain binding capacity was not normalized until after 6 days of K‐repletion. In mammalian skeletal muscle, K‐depletion leads to a marked and reversible reduction in 3H‐ouabain binding capacity, which may be secondary to the selective loss of K or gain of Na.
|Acta Physiologica Scandinavica
|Udgivet - okt. 1984