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absorption in
proximal tubule of neuronal nitric oxide synthase-knockout mice
1 Departments of Cellular and Molecular Physiology and 2 Department of Neurology, Yale University School of Medicine, New Haven, Connecticut 06520
Using
renal clearance techniques and in situ microperfusion of proximal
tubules, we examined the effects of
NG-monomethyl-L-arginine methyl
ester (L-NAME) on fluid and HCO3
transport in wild-type mice and also investigated proximal tubule transport in neuronal nitric oxide synthase (nNOS)-knockout mice. In
wild-type mice, administration of L-NAME (3 mg/kg bolus iv) significantly increased mean blood pressure, urine volume, and urinary
Na+ excretion. L-NAME, given by intravenous
bolus and added to the luminal perfusion solution, decreased absorption
of fluid (60%) and HCO3 (49%) in the proximal
tubule. In nNOS-knockout mice, the urinary excretion of
HCO3 was significantly higher than in the wild-type
mice (3.12 ± 0.52 vs. 1.40 ± 0.33 mM) and the rates of
HCO3 and fluid absorption were 62 and 72% lower,
respectively. Both arterial blood HCO3 concentration
(20.7 vs. 25.7 mM) and blood pH (7.27 vs. 7.34) were lower, indicating
a significant metabolic acidosis in nNOS-knockout mice. Blood pressure
was lower in nNOS-knockout mice (76.2 ± 4.6 mmHg) than in
wild-type control animals (102.9 ± 8.4 mmHg); however, it
increased in response to L-NAME (125.5 ± 5.07 mmHg).
Plasma Na+ and K+ were not significantly
different from control values. Our data show that a large component of
HCO3 and fluid absorption in the proximal tubule is
controlled by nNOS. Mice without this isozyme are defective in
absorption of fluid and HCO3 in the proximal tubule
and develop metabolic acidosis, suggesting that nNOS plays an important
role in the regulation of acid-base balance.
bicarbonate; acid-base
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