Role of nitric oxide in modulating renal function and arterial pressure during chronic aldosterone excess

Abstract

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 ⋅ min−1for 7 days) in conscious, chronically instrumented control dogs ( n = 9) and in dogs ( n = 12) pretreated with the NO synthesis inhibitor N G-nitro-l-arginine methyl ester (l-NAME; 10 μg ⋅ kg−1 ⋅ min−1). 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 withl-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.