Apart from Na,K-ATPase, a second sodium pump, Na-stimulated, ^-independent ATPase (Na -ATPase) is expressed in proximal convoluted tubule of the mammalian kidney. The aim of this study was to develop a method of Na -ATPase assay based on the method previously used by us to measure Na ,K -ATPase activity (Acta Biochim Polon.; 2002, 49: 515-27). The ATPase activity was assayed as the amount of inorganic phosphate liberated from ATP by isolated microsomal fraction. Na -ATPase activity was calculated as the difference between the activities measured in the presence and in the absence of 50 mM NaCl. Na -ATPase activity was detected in the renal cortex (3.5 ± 0.2 ^mol phosphate/h per mg protein), but not in the renal medulla. Na -ATPase was not inhibited by ouabain or an H ,K -ATPase inhibitor, Sch 28080, but was almost completely blocked by 2 mM furosemide. Leptin administered intraperitoneally (1 mg/kg) decreased the Na ,K -ATPase activity in the renal medulla at 0.5 and 1 h by 22.1% and 27.1%, respectively, but had no effect on Na -ATPase in the renal cortex. Chronic hyperleptinemia induced by repeated subcutaneous leptin injections (0.25 mg/kg twice daily for 7 days) increased cortical Na,K-ATPase, medullary Na,K-ATPase and cortical Na+-ATPase by 32.4%, 84.2% and 62.9%, respectively. In rats with dietary-induced obesity, the Na ,K - ATPase activity was higher in the renal cortex and medulla by 19.7% and 34.3%, respectively, but Na -ATPase was not different from control. These data indicate that both renal Na -dependent ATPases are separately regulated and that up-regulation of Na -ATPase may contribute to Na retention and arterial hypertension induced by chronic hyperleptinemia.
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