[Role of tubular Na-K-ATPase in nephrotic syndrome induced by puromycin in the rat]

Abstract

Na-K-ATPase is an ubiquitous enzyme involved in the tubular reabsorption process. Na-K-ATPase is specifically controlled in each nephron segment. Sodium retention is one of the main features of the nephrotic syndrome. Hypervolemia is found in most of the nephrotic syndromes in adults, suggesting a primary renal origin. In the puromycin-induced nephrotic syndrome in rats, the collecting duct is the site of sodium retention. We have shown that Na-K-ATPase activity is specifically enhanced in collecting ducts from rats with puromycin-induced nephrotic syndrome. The stimulation of Na-K-ATPase activity was independent of aldosterone and endogenous inhibitors of the Na-K-ATPase, suggesting a primary paracrin or cellular mechanism. We have demonstrated that two different isoforms of the Na-K-ATPase are coexpressed all along the rat nephron. In the puromycin-induced nephrotic syndrome, the activity of one isoform is specifically enhanced. These results demonstrate that the different isoforms of the Na-K-ATPase can be individually controlled.