Patterns of Acid–Base Regulation During Exposure to Hypercarbia in Fishes

Abstract

Acid–base regulation is one of the most tightly regulated physiological processes among vertebrates, and the specific mechanisms and patterns of acid–base regulation in fish have been investigated for decades, although primarily on a few species of teleosts and elasmobranchs. The most common response observed in fish during short-term (up to 96 h) exposure to hypercarbia is that of blood pH compensation for the induced respiratory acidosis by a net increase in plasma ${\rm HCO}_3^{-}$ in exchange for Cl⁻, predominantly through processes at the gills. Studies on hagfish indicate that this pattern of pH compensation (i.e. net plasma ${\rm HCO}_3^-/{\rm Cl}^-$ exchange, driving pH recovery) probably represents the ancestral state for fishes. Due to an apparent limit to this net ${\rm HCO}_3^-/{\rm Cl}^-$ exchange, most fishes examined to date exhibit incomplete pH compensation for the acidosis, in both plasma and tissues associated with CO₂ tensions greater than 10–16 mmHg; in CO₂-sensitive fishes, this may be the basis for mortality during exposure to high CO₂. A few fish species, however, are capable of tolerating PaCO₂s well above 10–16 mmHg; in some of these species, this tolerance appears to be associated with the ability to completely regulate intracellular pH (preferential pHi regulation) of tissues, such as brain, muscle and liver, despite a large reduction in extracellular pH. We hypothesize that: (a) preferential pHi regulation in fish evolved in the ancestors of the pleisiomorphic freshwater (non-teleost) actinopterygiians, (b) is associated with high CO₂ tolerance, and (c)was an exaptation for air-breathing. A great deal of research remains to test these hypotheses, and to elucidate the origin and ubiquity of preferential pHi regulation among fishes and the cellular and molecular mechanisms involved.