Submitted on March 31, 2008
Revised on June 10, 2008
Accepted on July 11, 2008
Blockade of Renal Medullary Bradykinin B2 Receptors Increases Tubular Sodium Reabsorption in Rats Fed a Normal Salt Diet
Sema-Hayriye Sivritas1, David W Ploth1, and Wayne R Fitzgibbon1*
1 Medical University of South Carolina
* To whom correspondence should be addressed. E-mail: fitzgiwr{at}musc.edu.
The present study was performed to test the hypothesis that under normal physiological conditions and/or during augmentation of kinin levels, intra-renal kinins act on medullary bradykinin B2 (BKB2) receptors to acutely increase papillary blood flow and therefore sodium 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, 2 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 changed to either 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 (UNaV) and fractional Na+ excretion by 40 ± 5% and 40 ± 4%, respectively (p<0.01), but did not alter glomerular filtration rate (GFR), papillary blood flow (PBF) or cortical blood flow (CBF). 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 BK B2 receptors to increase sodium excretion independent of changes in inner medullary blood flow.
