Background. The architecture of the vasa rectae produces significant oxygen
(O-2) "shunting" and marked decreases in renal medullary pO(2) values. We
hypothesized that carbon dioxide (CO2) trapping and increases in medullary
pCO(2) along with decreases in medullary pH values should also accompany th
is O-2 shunting.
Methods. We developed computer simulations employing a model of gas exchang
e through the countercurrent vasculature that predicted trapping of CO2 alo
ng with O-2 shunting. To test the validity of this model directly, medullar
y pH was measured by using needle electrodes in the in situ kidney before a
nd after the administration of mannitol or furosemide, or by decreasing blo
od flow with a transient decrease of renal perfusion pressure with a suprar
enal clamp. Data are expressed as mean +/- so.
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 w
ithin the kidney parenchyma. This gradient is related to the metabolic acti
vity of the thick ascending limb of Henle and the countercurrent vascular a
rchitecture, and may be relevant to a variety of physiological phenomena in
volved in volume, electrolyte, and acid-based homeostasis.