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/) mice in
vivo
Departments of 1 Physiology and Biophysics, 2 Comparative Medicine, and 3 Anesthesiology, Schools of Medicine and Dentistry, University of Alabama at Birmingham, Birmingham, Alabama 35294
The extent to which
endogenously generated nitric oxide alters Na+ transport
across the mammalian alveolar epithelium in vivo has not been
documented. Herein we measured alveolar fluid clearance and nasal
potential differences in mice lacking the inducible form of nitric
oxide synthase [iNOS; iNOS(
/)] and their corresponding wild-type
controls [iNOS(+/+)]. Alveolar fluid clearance values in iNOS(+/+)
and iNOS(/) anesthetized mice with normal oxygenation and acid-base
balance were ~30% of instilled fluid/30 min. In both groups of mice,
fluid absorption was dependent on vectorial Na+ movement.
Amiloride (1.5 mM) decreased alveolar fluid clearance in iNOS(+/+) mice
by 61%, whereas forskolin (50 µM) increased alveolar fluid clearance
by 55% by stimulating amiloride-insensitive pathways. Neither agent
altered alveolar fluid clearance in iNOS(/) mice. Hyperoxia
upregulated iNOS expression in iNOS(+/+) mice and decreased their
amiloride-sensitive component of alveolar fluid clearance but had no
effect on the corresponding values in iNOS(/) mice. Nasal potential
difference measurements were consistent with alveolar fluid clearance
in that both groups of mice had similar baseline values, which were
amiloride sensitive in the iNOS(+/+) but not in the iNOS(/) mice.
These data suggest that nitric oxide produced by iNOS under basal
conditions plays an important role in regulating amiloride-sensitive
Na+ channels in alveolar and airway epithelia.
nitric oxide; osmolality; hyperoxia; nasal potential difference; inducible nitric oxide synthase-deficient mice
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