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Articles in PresS, published online ahead of print May 29, 2002
Am J Physiol Renal Physiol, 10.1152/ajprenal.00243.2001
Submitted on August 1, 2001
Accepted on May 17, 2002
1 Department of Cellular and Molecular Physiology, Yale University School of Medicine, New Have, CT, USA
* To whom correspondence should be addressed. E-mail: tong.wang{at}yale.edu.
We have previously shown that mice lacking neuronal nitric oxide synthase (nNOS) are defective in absorption of fluid and bicarbonate in the proximal tubule, and develop metabolic acidosis. In the present study we examined the transport of fluid and bicarbonate in the proximal tubule and acid-base status in mice lacking two other isoforms of nitric oxide synthase; iNOS (inducible) and eNOS (endothelial). Proximal tubules were microperfused in situ in wild-type and NOS knockout mice by methods previously described (30). 3H-inulin and total CO2 concentrations were measured in the perfusate and collected fluid, and Jv and JHCO3 analyzed. Our data show that JHCO3 was 35% lower (71.7 ± 6.4 vs. 109.9 ± 7.3 pmole/min/mm, n=13, P < 0.01) and Jv was 38% lower (0.95 ± 0.15 vs. 1.54 ± 0.17 nl/min/mm 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 (L-NIL), 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 pmole/min/mm) and Jv (1.56 ± 0.17 vs. 1.55 ± 0.16 nl/min/mm) did not change significantly in eNOS knockout mice. These results indicated that iNOS upregulates Na+ and HCO3- transport, whereas eNOS does not direct modulate Na+ and HCO3- in the kidney proximal tubules.
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