Background: The architecture of the vasa rectae produces significant oxygen (O2) "shunting" and marked decreases in renal medullary pO2 values. We hypothesized that carbon dioxide (CO2) trapping and increases in medullary pCO2 along with decreases in medullary pH values should also accompany this O2 shunting.
Methods: We developed computer simulations employing a model of gas exchange through the countercurrent vasculature that predicted trapping of CO2 along with O2 shunting. To test the validity of this model directly, medullary pH was measured by using needle electrodes in the in situ kidney before and after the administration of mannitol or furosemide, or by decreasing blood flow with a transient decrease of renal perfusion pressure with a suprarenal clamp. Data are expressed as mean +/- SD.
Results: Medullary pH was lower than cortical pH (7.20 +/- 0.09 vs. 7.39 +/- 0.08, P < 0.01). Mannitol caused a decrease in medullary pH to 7.02 +/- 0.07 (P < 0.01), whereas furosemide increased medullary pH to 7. 31 +/- 0.09 (P < 0.01). Brief periods of severe hypotension decreased medullary pH to 6.90 +/- 0.09 (P < 0.01).
Conclusions: These data demonstrate that a significant pH gradient exists within the kidney parenchyma. This gradient is related to the metabolic activity of the thick ascending limb of Henle and the countercurrent vascular architecture, and may be relevant to a variety of physiological phenomena involved in volume, electrolyte, and acid-based homeostasis.