ROLE OF RENAL INTERSTITIAL PRESSURE AS A MEDIATOR OF SODIUM RETENTIONDURING 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 ef fects of intravenous NG-nitro-L-arginine-methyl ester (L-NAME), a synt hesis inhibitor, on renal hemodynamics, renal interstitial hydrostatic pressure, and sodium and lithium excretion were determined. L-NAME (5 0 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 para llel with systemic arterial pressure and in rats (n=8) in which renal perfusion pressure was servocontrolled constant at basal levels. Infus ion of L-NAME raised renal perfusion pressure from 122+/-6 to 157+/-4 mm Hg in the nonservocontrolled group but not in the servocontrolled g roup (118+/-3 mm Hg). L-NAME decreased renal plasma flow and glomerula r filtration rate to the same level in both rat groups. L-NAME signifi cantly 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 ex cretion 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 differen ce in the renal hemodynamic and excretory responses to L-NAME between the servocontrolled and nonservocontrolled groups. In summary, reducti ons in sodium excretion during inhibition of nitric oxide synthesis ar e associated with significant reductions in renal interstitial hydrost atic pressure. Similar responses in sodium excretion and renal interst itial hydrostatic pressure to L-NAME between servocontrolled and nonse rvocontrolled groups indicate blunted pressure natriuresis and reduced transmission of renal perfusion pressure into renal interstitium duri ng nitric oxide blockade. These data indicate that decreases in renal interstitial hydrostatic pressure may, in part, play a role in mediati ng the sodium retention of nitric oxide blockade.