Na (+) -K (+) -ATPase activity: role in the impaired sodium excretion of experimental nephrosis in rats
Lu, S.G.; Jiang, X.Y.; Hu, M.C.; Guo, M.
Chinese Medical Journal 107(7): 536-540
1994
ISSN/ISBN: 0366-6999 PMID: 7956502 Document Number: 436668
Using the model of adriamycin-induced nephrotic syndrome in rats, we studied the relationship between urine electrolyte excretion rates and proteinuria and determined the activity of Na(+)-K(+)-ATPase in the renal tissue of nephrotic rats. No relationship was found between the increased sodium reabsorption and proteinuria. But the impaired salt excretion was inversely related to the increase of Na(+)-K(+)-ATPase activity in the renal inner medulla. It is proposed that direct effect of adriamycin on renal tubule cells is the primary events, that the increased Na(+)-ATPase activity on basolateral membrane of renal tubule cells be an intrarenal factor which mediates the action of retention of salt by the kidney and that inner medullary collecting ducts might be one of the sites of the sodium retention in nephrotic rats.