DOES BASAL PRODUCTION OF NITRIC-OXIDE CONTRIBUTE TO REGULATION OF BRAIN-FLUID BALANCE

Nitric oxide (NO), or a NO-containing compound, appears to mediate endothelium-dependent relaxation and may influence resting vascular tone. The goal of the present study was to examine the hypothesis that formation of NO has an important influence on blood flow to the brain and the choroid plexus. We measured blood flow with microspheres in anesthetized rabbits. Intravenous injection of N(G)-nitro-L-arginine (L-NNA, 3 and 30 mg/kg), an analogue of arginine that inhibits the enzymatic formation of NO, had no significant effect on cerebral blood flow. Arterial pressure was maintained at control levels after injection of L-NNA. In contrast, L-NNA decreased blood flow to the choroid plexus by 36 +/- 4 (mean +/- SE) and 51 +/- 8% (P < 0.05 for both doses), respectively, from a control value of 563 +/- 77 ml.min-1.100 g-1. L-NNA also reduced blood flow to the kidney, but the effect tended to be less than that observed in the choroid plexus. Decreases in blood flow to the choroid plexus and kidney were inhibited by pretreatment with L-arginine (60 mg.kg-1.min-1). L-Arginine alone had little effect on blood flow to the choroid plexus, brain, or kidney. These findings suggest that NO, or a closely related compound, derived from L-arginine has important effects on basal perfusion of the choroid plexus, the major site of formation of cerebrospinal fluid.