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

Abstract

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 ∼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.

Summary

White sturgeon were exposed to two levels of elevated CO₂ (1 and 4 kPa) in water of two different pH values, and we tracked pH compensatory responses over the following two days. Acidifying water at modest CO₂ levels within the limit for complete compensation reduced the rate at which blood pH recovered. Alkalizing water during severe hypercapnia typically beyond that limit increased both the magnitude and the rate of organismal pH compensation. Intracellular pH protection was unaffected by any treatment.