ROLE OF RENAL INTERSTITIAL PRESSURE AS A MEDIATOR OF SODIUM RETENTION DURING SYSTEMIC BLOCKADE OF NITRIC-OXIDE

The role of renal interstitial pressure was examined in mediating the sodium retention induced by blockade of nitric oxide synthesis. The effects of intravenous NG-nitro-L-arginine-methyl ester (L-NAME), a synthesis inhibitor, on renal hemodynamics, renal interstitial hydrostatic pressure, and sodium and lithium excretion were determined. L-NAME (50 mug/kg per minute) was infused for 75 minutes in Sprague-Dawley rats (n=7) in which renal perfusion pressure was permitted to rise in parallel with systemic arterial pressure and in rats (n=8) in which renal perfusion pressure was servocontrolled constant at basal levels. Infusion of L-NAME raised renal perfusion pressure from 122+/-6 to 157+/-4 mm Hg in the nonservocontrolled group but not in the servocontrolled group (118+/-3 mm Hg). L-NAME decreased renal plasma flow and glomerular filtration rate to the same level in both rat groups. L-NAME significantly decreased sodium excretion (1.38+/-0.41 to 0.36+/-0.14 muEq/min and 1.19+/-0.46 to 0.30+/-0.05 muEq/min, respectively), fractional excretion of lithium (25.7+/-1.7% to 16.7+/-2.3% and 25.6+/-4.0% to 18.2+/-1.7%), and renal interstitial hydrostatic pressure (6.4+/-1.4 to 3.2+/-0.9 mm Hg and 6.3+/-1.8 to 2.7+/-0.9 mm Hg) in servocontrolled and nonservocontrolled groups. However, there was no significant difference in the renal hemodynamic and excretory responses to L-NAME between the servocontrolled and nonservocontrolled groups. In summary, reductions in sodium excretion during inhibition of nitric oxide synthesis are associated with significant reductions in renal interstitial hydrostatic pressure. Similar responses in sodium excretion and renal interstitial hydrostatic pressure to L-NAME between servocontrolled and nonservocontrolled groups indicate blunted pressure natriuresis and reduced transmission of renal perfusion pressure into renal interstitium during nitric oxide blockade. These data indicate that decreases in renal interstitial hydrostatic pressure may, in part, play a role in mediating the sodium retention of nitric oxide blockade.