Transepithelial ion transfer processes as mechanisms for fish acid–base regulation in hypercapnia and lactacidosis

Abstract

In fish, the respiratory acidosis resultant from environmental hypercapnia is generally compensated by bicarbonate accumulation in intracellular and extracellular body compartments. The additional bicarbonate is partially produced by nonbicarbonate buffering, but primarily gained from the environment via rate-limited ion transfer mechanisms, which apparently are dependent upon certain environmental factors. During lactacidosis resultant from strenuous exercise the majority of produced H+ ions is initially buffered intracellularly, until they are transiently transferred via ion exchange mechanisms to the environment. After normalization of the acid–base status (at still high intracorporal lactate levels) H+ ions are gradually recovered from the water for further aerobic processing of lactic acid.In both types of acid–base disturbances, ion exchanges effective for the acid–base status are primarily performed via the branchial epithelium. The role of the fish kidneys is usually small; skin and other excretory sites contribute only insignificantly.Branchial transfer of surplus H+ ions by fish to the environment appears to be a very common and probably the most important mechanism utilized to cope with severe acid–base disturbances, thereby mitigating against the effects of adverse environmental conditions on their "milieu interieur."