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Am J Physiol Renal Physiol 283: F658-F662, 2002. First published May 29, 2002; doi:10.1152/ajprenal.00243.2001
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Vol. 283, Issue 4, F658-F662, October 2002

Role of iNOS and eNOS in modulating proximal tubule transport and acid-base balance

Tong Wang

Department of Cellular and Molecular Physiology, Yale University School of Medicine, New Haven, Connecticut 06520

Our laboratory has previously shown that mice lacking neuronal nitric oxide synthase (nNOS) are defective in fluid absorption (Jv) and HCO<UP><SUB>3</SUB><SUP>−</SUP></UP> absorption (JHCO3) in the proximal tubule and develop metabolic acidosis. The present study examined the transport of fluid and HCO<UP><SUB>3</SUB><SUP>−</SUP></UP> in the proximal tubule and acid-base status in mice lacking two other isoforms of NOS, inducible NOS (iNOS) and endothelial NOS (eNOS). Proximal tubules were microperfused in situ in wild-type and NOS knockout mice by methods previously described (Wang T, Yang C-L, Abbiati T, Schultheis PJ, Shull GE, Giebisch G, and Aronson PS. Am J Physiol Renal Physiol 277: F298-F302, 1999). [3H]inulin and total CO2 concentrations were measured in the perfusate and collected fluid, and net Jv and JHCO3 were analyzed. These data show that JHCO3 was 35% lower (71.7 ± 6.4 vs. 109.9 ± 7.3 pmol · min-1 · mm-1, n = 13, P < 0.01) and Jv was 38% lower (0.95 ± 0.15 vs. 1.54 ± 0.17 nl · min-1 · mm-1, n = 13, P < 0.05) in iNOS knockout mice compared with their wild-type controls. Addition of the iNOS-selective inhibitor L-N6-(1-iminoethyl) lysine, reduced both Jv and JHCO3 significantly in wild-type, but not in iNOS knockout, mice. In contrast, both JHCO3 (93.3 ± 7.9 vs. 110.6 ± 6.18 pmol · min-1 · mm-1) and Jv (1.56 ± 0.17 vs. 1.55 ± 0.16 nl · min-1 · mm-1) did not change significantly in eNOS knockout mice. These results indicated that iNOS upregulates Na+ and HCO<UP><SUB>3</SUB><SUP>−</SUP></UP> transport, whereas eNOS does not directly modulate Na+ and HCO<UP><SUB>3</SUB><SUP>−</SUP></UP> transport in the kidney proximal tubules.

nitric oxide synthase; inducible nitric oxide synthase; endothelial nitric oxide synthase; neuronal nitric oxide synthase; knockout mice; kidney tubule; transport


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