Atrial natriuretic peptide induces sustained natriuresis in conscious dogs

Although acute infusions of atrial natriuretic peptide (ANP) often cause natriuresis, these effects are not sustained, possibly because of reductions in arterial pressure or other compensatory adaptations. The aim of this study was to determine whether physiological increases in intrarenal ANP levels cause sustained natriuresis if changes in arterial pressure and other neurohumoral influences that might obscure the renal responses are controlled. Changes in renal function were quantitated during chronic unilateral renal arterial infusion of ANP at rates of 1, 2, and 4 ng·kg^-1·min^-1 in conscious dogs (n = 7) with the urinary bladder split to allow continuous measurement of renal excretion in the ANP-infused and contralateral, vehicle-infused kidneys. There was no change in mean arterial pressure at any infusion rate. During 1 ng·kg^-1·min^-1 infusion of ANP for 5 days, the renal excretory responses were small and variable. However, during 2 and 4 ng·kg^-1·min^-1 ANP infusion for 7 days, sodium excretion averaged 37.2 ± 10.0 and 134.8 ± 19.0% greater, respectively, in the ANP-infused kidneys compared with the vehicle-infused kidneys but there were no changes in glomerular filtration rate or effective renal plasma flow. These results demonstrate that when compensatory changes in arterial pressure and neurohumoral factors are controlled, ANP, at physiological concentrations, causes marked increases in renal excretion. This study supports the concept that ANP's effects to increase renal excretory capability could play a role in long-term control of arterial pressure and body fluid homeostasis.