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Am J Physiol Renal Physiol 295: F811-F817, 2008. First published July 16, 2008; doi:10.1152/ajprenal.90225.2008
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Blockade of renal medullary bradykinin B2 receptors increases tubular sodium reabsorption in rats fed a normal-salt diet

Sema-Hayriye Sivritas, David W. Ploth, and Wayne R. Fitzgibbon

Division of Nephrology, Department of Medicine, Medical University of South Carolina, Charleston, South Carolina

Submitted 31 March 2008 ; accepted in final form 11 July 2008

The present study was performed to test the hypothesis that under normal physiological conditions and/or during augmentation of kinin levels, intrarenal kinins act on medullary bradykinin B2 (BKB2) receptors to acutely increase papillary blood flow (PBF) and therefore Na+ excretion. We determined the effect of acute inner medullary interstitial (IMI) BKB2 receptor blockade on renal hemodynamics and excretory function in rats fed either a normal (0.23%)- or a low (0.08%)-NaCl diet. For each NaCl diet, two groups of rats were studied. Baseline renal hemodynamic and excretory function were determined during IMI infusion of 0.9% NaCl into the left kidney. The infusion was then either changed to HOE-140 (100 µg·kg–1·h–1, treated group) or maintained with 0.9% NaCl (time control group), and the parameters were again determined. In rats fed a normal-salt diet, HOE-140 infusion decreased left kidney Na+ excretion (urinary Na+ extraction rate) and fractional Na+ excretion by 40 ± 5% and 40 ± 4%, respectively (P < 0.01), but did not alter glomerular filtration rate, inner medullary blood flow (PBF), or cortical blood flow. In rats fed a low-salt diet, HOE-140 infusion did not alter renal regional hemodynamics or excretory function. We conclude that in rats fed a normal-salt diet, kinins act tonically via medullary BKB2 receptors to increase Na+ excretion independent of changes in inner medullary blood flow.

inner medullary collecting duct; inner medullary blood flow; renal hemodynamics; renal excretion



Address for reprint requests and other correspondence: W. R. Fitzgibbon, Dept. of Medicine, Div. of Nephrology, Medical Univ. of South Carolina, 96 Jonathan Lucas St., PO Box 250623, Charleston, SC 29425 (e-mail: fitzgiwr{at}musc.edu)







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