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

Chronic aldosterone (Aldo) excess is associated with transient sodium reten tion, extracellular fluid volume expansion, renal vasodilation, and hyperte nsion. 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-ret aining actions of Aldo. To achieve this goal, we examined the long-term eff ects of Aldo (15 mu g.kg(-1).min(-1) 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 mu g.kg (-1).min(-1)). In control dogs, Aldo caused a transient sodium retention (1 26 +/- 6 to 56 +/- 2 meq/day) followed by a return of sodium excretion to n ormal levels. Aldo also increased renal plasma flow by 15% (205 +/- 13 to 2 33 +/- 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 increa sed 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 pretr eated with L-NAME compared with control, the renal hemodynamic response was markedly attenuated. The results of this study suggest that NO plays an im portant role in mediating the renal vasodilation during chronic Aldo excess .