Article Text

  1. S. H. Sivritas,
  2. D. W. Ploth,
  3. W. R. Fitzgibbon
  1. Division of Nephrology, Department of Medicine, Medical University of South Carolina, Charleston, SC


The finding that infusion of bradykinin into the renal medullary interstitium increases both sodium excretion and medullary blood flow and that both sodium excretion and medullary blood flow are decreased by blockade of intrarenal bradykinin B2 receptors has led to the proposal that medullary kinins regulate electrolyte reabsorption indirectly by altering medullary blood flow. We tested this proposal by examining the effect of acute inner medullary interstitial (IMI) bradykinin B2 receptor blockade on urinary Na excretion (UNaV) and renal hemodynamics in anesthetized Sprague-Dawley rats. A catheter was tunneled into the IMI for the infusion of 0.9% NaCl or HOE 140 at 0.16 mL/h. A laser Doppler fiber probe was also tunneled into the IMI and a second laser Doppler probe was placed on the surface of the kidney. An ultrasonic Doppler probe was then placed on the renal artery. Two groups of rats were studied. Baseline mean arterial pressure (MAP), urinary flow rate (Uv), UNaV, cortical (CBF), and inner medullary (MBF) and renal blood flows (RBF) were determined during infusion of 0.9% NaCl. The infusion was then changed to either HOE 140 (100 μg/kg/h, n = 8) or maintained with 0.9% NaCl (time control, n = 10). Following a 20 min stabilization period the parameters were again determined. Infusion of HOE 140 did not alter MAP. In contrast, HOE 140 infusion decreased Uv (5.49 6 0.48 vs 4.74 6 0.41 μL/min/g kwt for baseline and HOE 140 periods respectively, p < .05). Further, HOE infusion decreased UNaV by 38 6 5% (p < .05). This change in UNaV was greater (p < .05) than that observed for the rats in the time control group (22 6 11%). Infusion of HOE into the IMI did not alter RBF (6.16 6 0.33 vs 5.88 6 0.26 mL/min/g kwt), MBF (43.8 6 1.9 vs 44.0 {38} 2.2 units), or CBF (447.4 6 17.7 vs 446.7 6 16.5 units). Our findings indicate that medullary bradykinin B2 receptor blockade decreases sodium excretion in the absence of a change in inner medullary blood flow. We conclude that in rats fed a normal salt intake medullary kinins act tonically to increase sodium excretion. This effect appears to be independent of changes in medullary blood flow.

This work was supported by NIH grant no. C06 RR015455 from the Extramural Research Facilities program of the NCRR.

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