Blockade of renal medullary bradykinin B2receptors increases tubular sodium reabsorption in rats fed a normal-salt diet

Abstract

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) BKB2receptor 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 BKB2receptors to increase Na+excretion independent of changes in inner medullary blood flow.