Water pH alters acid-base compensatory responses in white sturgeon (Acipenser transmontanus) exposed to modest and severe environmental hypercapnia

Elevated CO2 (hypercapnia) in fishes induces a respiratory acidosis, which is compensated by branchial acid-base relevant ion transfer. This organismal compensation is hypothesized to be affected by water pH, but assessing this effect is difficult when examining fish species (e.g., rainbow trout Oncorhynchus mykiss, Japanese flounder, Paralichthys olivaceus) that rely on extracellular pH regulation (pHe) to drive recovery as when it fails, mortality may occur quickly. Examining fishes that both perform pHe compensation, but do not require it for survival due to preferential intracellular pH (pH(i)) regulation (PPR) such as does the white sturgeon (Acipenser transmontanus), allows us to determine the effect of water pH on acid-base compensation during hypercapnia. White sturgeon were exposed to 48 h of elevated CO2 tensions while manipulating water pH to determine how water pH can alter patterns of acid-base compensation. Our findings demonstrate that water pH manipulation can have significant effects on the pHe compensatory response. For example, complete pHe compensation was observed in fish exposed to water equilibrated with 1 kPa CO2, but reducing water pH by similar to 1 pH unit prevented complete compensation. Alternately, when sturgeon were exposed to alkalized water equilibrated with 4 kPa CO2 (i.e., pH of 6.3 compared to 5.7 for water with 4 kPa CO2), pH compensation was more rapid. Water pH and pHe compensation rates had no effect on pH(i) regulation. Our findings demonstrate that water pH can aid or assist pHe compensatory rates at a range of hypercapnic challenges, and so may have contributed to the origin of PPR as a primary strategy for some fish species to protect critical tissues largely independent of environmental conditions.