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Department of Physiology and Biophysics and The Center for Excellence in Cardiovascular-Renal Research, University of Mississippi Medical Center, Jackson, Mississippi 39216-4505
Chronic
aldosterone (Aldo) excess is associated with transient
sodium retention, extracellular fluid volume expansion, renal vasodilation, and hypertension. The purpose of this study was to
determine the role of nitric oxide (NO) in mediating the renal vasodilation and the escape from the sodium-retaining actions of Aldo.
To achieve this goal, we examined the long-term effects of Aldo (15 µg · kg
1 · min1
for 7 days) in conscious, chronically instrumented control dogs (n = 9) and in dogs
(n = 12) pretreated with the NO
synthesis inhibitor
NG-nitro-L-arginine methyl ester
(L-NAME; 10 µg · kg1 · min1).
In control dogs, Aldo caused a transient sodium retention (126 ± 6 to 56 ± 2 meq/day) followed by a return of sodium excretion to
normal levels. Aldo also increased renal plasma flow by 15% (205 ± 13 to 233 ± 16 ml/min), glomerular filtration rate by 20% (72 ± 3 to 87 ± 5 ml/min), and arterial pressure from 90 ± 3 to 102 ± 3 mmHg. Aldo increased urinary nitrate/nitrite excretion by
60% in the control dogs. Although the sodium-retaining (144 ± 7 to
56 ± 7 meq/day) and arterial pressure (122 ± 6 to 136 ± 5 mmHg) responses to Aldo were the same in dogs pretreated with L-NAME compared
with control, the renal hemodynamic response was markedly attenuated.
The results of this study suggest that NO plays an important role in
mediating the renal vasodilation during chronic Aldo excess.
endothelium; kidney; hypertension
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