Dissociation of CO2 hydration and renal acid secretion in the dogfish, Squalus acanthias.

Abstract

Maximal rates of renal hydrogen ion secretion and bicarbonate reabsorption in the dogfish were stimulated by intravascular infusion of acidic and basic buffers: bicarbonate, phosphate, phenol red, dimethadione (DMO), imidazole, and piperazine-N,N'-bis(2 ethanesulfonic acid) (PIPES). There was no difference in titratable acid secretion or urinary pH after bicarbonate infusion despite a sevenfold increase in plasma bicarbonate. Bicarbonate reabsorption was increased 12-fold and showed no evidence of reaching a maximum. This was not altered by methazolamide, as expected, since there is no renal carbonic anhydrase in seagoing fish. Imidazole resulted in the greatest augmentation of renal titratable acid secretion (33----390 mueq . h-1 . kg-1) and did not alter urinary pH. Inhibition of organic base secretion by Darstine had no effect on the imidazole-induced maximal rate of acid secretion. This rate was compared with that of hydrogen ion generation calculated from the uncatalyzed reactions of CO2 and H2O or OH-, maximizing PCO2 and OH- gradients and reaction volumes in vivo. These calculated chemical rates could only account for 9-14% of the measured maximal acidification rate. Thus the powerful process that maintains constant acid urine pH is not only independent of carbonic anhydrase but can function well in a low CO2 environment in which the reactions CO2 + H2O or CO2 + OH- do not furnish enough protons for H+ secretion or HCO3- reabsorption. We conclude that following the cellular protolysis of water, processes other than those involving CO2 buffering of OH- permit H+ to engage in the formation of urine.