PERFUSION-PRESSURE AND VOLUME STATUS DETERMINE THE MICROVASCULAR RESPONSE OF THE RAT-KIDNEY TO N-G-MONOMETHYL-L-ARGININE

This study investigated the role of volume status and perfusion pressu re on the hemodynamic response of cortical and medullary renal capilla ries to systemic inhibition of nitric oxide. N-G-Monomethyl-L-arginine (L-NMMA) was infused intravenously (15-mg/kg bolus and 500-mu g.min(- 1).kg(-1) infusion), and blood flow in cortical capillaries (Q(CC)) an d in descending (Q(DVR)) and ascending vasa recta (Q(AVR)) was measure d by fluorescence videomicroscopy in euvolemic and volume-expanded ane sthetized Munich-Wistar rats. L-NMMA in euvolemic rats decreased vasa recta blood flow (Delta Q(DVR), 3.97 +/- 0.80 nL/min [P < .01]; Delta Q(AVR), 1.90 +/- 0.39 nL/min [P < .01]; n = 6) and Q(CC) (Delta Q(CC), 0.57 +/- 0.15 nL/min [P < .01]; n = 7) despite increases in renal per fusion pressure (RPP). Fractional excretion of sodium (FE(Na)) remaine d unchanged. In volume-expanded rats, L-NMMA decreased vasa recta bloo d flow when RPP increased (Delta Q(DVR), 1.42 +/- 0.79 nL/min [P = .05 ]; Delta Q(AVR), 1.95 +/- 0.34 nL/min [P < .001]; n = 9) or was held c onstant by partial aortic occlusion (Delta Q(DVR), 1.19 +/- 0.45 nL/mi n [P < .05]; Delta Q(AVR), 1.44 +/- 0.40 nL/min [P < .01]; n = 8). Q(C C) was unchanged by L-NMMA when RPP increased (Delta Q(CC), 0.27 +/- 0 .20 nL/min; n = 8) but decreased significantly by 0.61 +/- 0.11 nL/min (P < .01, n = 8) when increases in RPP were prevented. FE(Na) increas ed when RPP increased (Delta FE(Na), 2.47 +/- 0.51%; P < .001) and was held constant (Delta FE(Na), 2.64 +/- 0.46%; P < .001). In summary, s ystemic inhibition of nitric oxide increases blood pressure while decr easing Q(CC) and medullary capillary blood how in euvolemic rats. In v olume-expanded rats, L-NMMA again increases blood pressure but selecti vely decreases medullary blood flow without changing Q(CC); Q(CC) decr eased, however, when RPP was held constant. This study supports a role for nitric oxide synthesis in the regulation of Q(CC) and medullary b lood flow and demonstrates that volume expansion allows increases in R PP to maintain Q(CC) but not medullary blood flow during inhibition of nitric oxide.