Role of Nitric Oxide on Papillary Blood Flow and Pressure Natriuresis

Abstract

Abstract This study examined whether nitric oxide synthesis blockade or potentiation (with N ^ω -nitro- l- arginine methyl ester [L-NAME] or N -acetylcysteine, respectively) can shift the relations between sodium excretion, papillary blood flow, and renal perfusion pressure. Papillary blood flow was measured by laser Doppler flowmetry. A low dose of L-NAME (3.7 nmol/kg per minute) reduced papillary blood flow only at high arterial pressure (140 mm Hg), but it had no effect on pressure natriuresis. Infusion of 37 nmol/kg per minute L-NAME reduced cortical blood flow by 9% at all perfusion pressures studied, lowered papillary blood flow by 8% and 19% at 120 and 140 mm Hg, respectively, and blunted the pressure-natriuresis response. The administration of 185 nmol/kg per minute L-NAME reduced cortical blood flow by 30% and decreased papillary blood flow by 25% in the range of 100 to 140 mm Hg of arterial pressure. Blockade of nitric oxide synthesis with L-NAME at all doses studied reduced papillary blood flow only at high renal perfusion pressures, but papillary blood flow remained essentially unchanged at low perfusion pressures, thus restoring papillary blood flow autoregulation. N -Acetylcysteine (1.8 mmol/kg) increased papillary blood flow by 9% and shifted the relations between papillary blood flow, sodium excretion, and renal perfusion pressure toward lower pressures. This effect of N -acetylcysteine on papillary blood flow was blocked by subsequent L-NAME administration. The results indicate that increases in renal medullary levels of nitric oxide as renal perfusion pressure rises may be responsible for the lack of renal medullary blood flow autoregulation and the pressure-natriuretic response in volume-expanded rats.