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1 Department of Medical Physiology, Texas A&M University System Health Science Center, College Station, Texas 77843-1114; and 2 Department of Medical Physiology, University of Copenhagen, DK-2200 Copenhagen N, Denmark
The renal effects of the nitric oxide (NO)
synthase inhibitor nitro-L-arginine methyl ester
(L-NAME) were investigated in conscious dogs undergoing
sustained water diuresis and replacement of urinary sodium losses.
Experiments were performed with and without additional extracellular
volume expansion (isotonic saline, 2% body wt). L-NAME (10 µg · kg
1 · min1) infused
during water diuresis decreased urine flow (2.5 ± 0.2 to 1.5 ± 0.3 ml/min), free water clearance (1.9 ± 0.2 to 1.0 ± 0.2 ml/min), and sodium excretion (4.0 ± 1.7 to 2.1 ± 0.6 µmol/min). Arterial blood pressure increased from 112 ± 2 to
126 ± 3 mmHg, but creatinine clearance did not measurably change.
Plasma endothelin and vasopressin concentrations and plasma renin
activity (PRA) were unchanged. Urinary endothelin concentration
increased (3.4 ± 0.8 to 6.2 ± 1.7 pg/ml), but the excretion
rate remained constant. L-Arginine infusion (0.6 mg · kg1 · min1) along with
L-NAME abolished the renal effects but not the blood pressure increase. Volume expansion increased urine flow (2.5 ± 0.4 to 5.7 ± 0.5 ml/min) and sodium excretion (3.8 ± 1.6 to 76.5 ± 14.5 µmol/min). L-NAME attenuated the renal
effects of volume expansion: urine flow increased to 2.8 ± 0.7 ml/min and sodium excretion to 34 ± 17 µmol/min. PRA decreased
with control volume expansion but not during L-NAME.
Urinary endothelin levels were elevated by L-NAME,
decreased with volume expansion in all series, but excretion rate
remained constant. Infusion of L-arginine partially
reversed these effects of L-NAME. The results demonstrate that NO synthase inhibition increases blood pressure and blunts the
renal responses to water and saline loading.
water diuresis; volume expansion; sodium excretion; endothelium-derived relaxing factor
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