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Department of Physiology, Tulane University School of Medicine, New Orleans, Louisiana 70112
Nitric oxide (NO) is
rapidly oxidized to nitrite (NO
2) and
then to nitrate (NO
3) in biological tissues. Although urinary excretion rates of
NO
3 are often used as an index of NO
production in the body, very little is known regarding the kidney's
ability to excrete circulating NO
3. We
have evaluated the renal responses to systemic administration of sodium
nitrate (NaNO3) in eight
anesthetized dogs treated with the NO synthase inhibitor,
nitro-L-arginine (NLA; 50 µg · kg
1 · min
1),
intrarenally to minimize renal production of NO. Urinary and plasma
concentrations of
NO
3/NO
2 (NOX) were determined by the Greiss reaction after enzymatic reduction of NO
3 to
NO
2. NLA treatment alone resulted in
reductions in urinary NOX excretion rates (UNOXV, 1.13 ± 0.2 to 0.53 ± 0.1 nmol · min
1 · g
1)
and an increase in fractional reabsorption of NOX (FRNOX,
93.8 ± 0.6 to 97 ± 0.6%) without changes in arterial plasma
concentrations (ANOX, 18.7 ± 1.4 to 21.2 ± 3.7 µM). Administration of NaNO3
(10, 20, 30, and 40 µg · kg
1 · min
1)
resulted in dose-dependent increases in ANOX (34.5 ± 8.0, 46.4 ± 7.3, 60.7 ± 6.3, and 78.1 ± 6.3 µM),
UNOXV (1.8 ± 0.7, 4.2 ± 1.8, 7.0 ± 2.0, and
11.4 ± 3.3 nmol · min
1 · g
1),
and decreases in FRNOX (93.8 ± 2.3, 90.3 ± 3.5, 88.6 ± 3.2, and 84.6 ± 3.5%). Absolute net tubular
reabsorption of NO
3 showed a linear
relationship with filtered loads, with no evidence of a transport
maximum. These data show that, in the absence of additions from
intrarenal sources, urinary excretion rates of nitrate increases
progressively in response to increases in its circulating levels
without exhibiting a transport maximum but with progressive decreases
in fractional reabsorption.
nitric oxide; plasma nitrate; tubular reabsorption; nitrate excretion
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