Deficiency of carbonic anhydrase in the vasculature of rabbit kidneys.

R M Effros; S Nioka

doi:10.1172/JCI110895

Deficiency of carbonic anhydrase in the vasculature of rabbit kidneys.

R M Effros and S Nioka

Published May 1, 1983 - More info

View PDF

Abstract

The transit of 14CO2 and H14CO3- through the renal vasculature was studied in rabbit kidneys perfused without erythrocytes and in an in vivo preparation in which erythrocytes were present. In the absence of erythrocytes, the transit of 14CO2 from the renal artery to renal vein was much more rapid than that of H14CO3-. This suggests that (a) there is insufficient carbonic anhydrase (c.a.) in the vasculature between the renal artery and the exchange vessels of the kidney to ensure equilibration between CO2 and HCO3- and (b) CO2 can diffuse directly between arterial and venous vessels in the kidney. Following infusions of carbonic anhydrase, the renal venous outflow patterns of 14CO2 and H14CO3- became the same in the perfused kidneys. Although the initial recovery of 14CO2 remained greater than that of H14CO3- after infusions of acetazolamide (a c.a. inhibitor), arteriovenous diffusion of 14CO2 was diminished by this agent. This is attributed to inhibition of renal tubular c.a. The outflow patterns of H14CO3- and 14CO2 were nearly the same in the presence of erythrocytes, indicating that erythrocyte c.a. is sufficiently accessible to permit virtual equilibration of these radionuclides during the interval required for transit between the renal artery and exchange vessels. However, addition of carbonic anhydrase to the plasma seemed to accelerate transit of both 14CO2 and H14CO3- through the kidneys, and a small disequilibrium between CO2 and HCO3- may therefore normally be present in the renal interstitium and capillaries.