Inhibition of Na+,K+-stimulated ATPase in the cochlea of the guinea pig. A potential cause of disturbed inner ear function in terminal renal failure.
The frequent occurrence of sensorineural hearing loss in patients with chronic renal insufficiency prompted us to study the influence of chronic renal failure upon Na+,K+-ATPase in the inner ear of guinea pigs. Na+,K+-activated ATPase was defined as the ouabain-sensitive part of total ATPase, the activity of which was obtained in the presence of sodium, potassium and magnesium. A significant reduction of Na+,K+-activated ATPase was found in the inner ear of uremic animals. Such inhibition could be demonstrated as early as 12 hours after subtotal nephrectomy. An inverse correlation was found between serum creatinine levels and Na+,K+-activated ATPase. A similar inhibition of Na+,K+-activated ATPase in uremia is also found in other tissues (erythrocytes, renal tubules, intestinal mucosal cells, sarcolemma). Na+,K+-ATPase in the cochlea plays a key role in the maintenance of cochlear cationic gradients. It is suggested that inhibition of this enzyme system may contribute to the inner ear dysfunction in uremia.
D000818:Animals; D001692:Biological Transport; D003051:Cochlea / Q000201:enzymology*; D003404:Creatinine / Q000097:blood; D006319:Hearing Loss, Sensorineural / Q000201:enzymology* / Q000209:etiology; D007676:Kidney Failure, Chronic / Q000150:complications* / Q000201:enzymology; D008297:Male; D051379:Mice; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism*; D014508:Urea / Q000097:blood
D014508:Urea; D003404:Creatinine; D000254:Sodium-Potassium-Exchanging ATPase