Blood acidification in the swimbladder: mechanisms and metabolic pathways

ABSTRACT

The metabolism of gas gland cells of the swimbladder epithelium is specialized for the production of acidic metabolites that are released into the blood stream and provoke an increase in gas partial pressure by reducing the effective gas-carrying capacity of the blood. In a subsequent step this initial increase in gas partial pressure is multiplied by back-diffusion of gas molecules from the venous to the arterial side in the countercurrent system, the rete mirabile. Thus, gas partial pressures of up to several hundred atmospheres can be generated in the swimbladder. Measurements of metabolic end products and analysis of the formation of 14C02 from [1-14(superscription) C] glucose and [6-14(superscription) C] glucose revealed that the acidic metabolises are lactic acid, produced in the glycolytic pathway, and also C02, formed in the pentose phosphate shunt. C02 easily enters the blood stream by diffusion. The release of protons from isolated gas gland cells, however, is highly dependent on the extracellular sodium concentration. This sodium dependence can in part be blocked by addition of amiloride, indicating that a Na+/ H+ exchanger is involved in the release of protons. A significant decrease in the rate of proton secretion in the presence of the carbonic anhydrase inhibitor ethoxzolamide indicates that the second major route for the release of protons includes carbonic anhydrase activity and the diffusion of C02.