Abstract

The acid-tolerant banded sunfish (Enneacanthus obesus) survived losses in body sodium, due to low pH, that would kill other species. Asplasma sodium concentration declined, aproportionate decline of plasma osmoticpressure occurred, followed by shrinkage of the extracellularfluid volume (ECFV). ECFV declined from 44% of the total body water at control pH to about 30% after 1 wk at pH 3.5. Enneacanthus obesus compensated for the lowpH-induced osmotic disturbance in several ways. With body salt depletion, sodium shifted from the slowly exchangeable pool (SEP), where it was osmotically inactive, into the rapidly exchangeable pool (REP), where it helped to maintain the extracellular fluid sodium concentration. About 88% of the total sodium in the fish at the control pH was in the REP. The proportion declined to about 81% after 2 d atpH 3.5, but returned to control levels by 14 d. Sodium in bone constitutes one-fifth of all the sodium in the fish and is an important component of the SEP. The sodium concentration of bone declined during acid exposure, which indicates that it may be a significant reservoir during depletion of body sodium. Decreases in body water content and body potassium concentration helped reduce movement of water from the extracellular fluid into the intracellular fluid. These compensatory changes took days, andpresumably accounted at leastpartially for acclimation efects on sodium balance. In contrast, the sizes of the REP and ECFV of E. obesus that died after 1–2 h at pH 2.95 increased to 100% of body sodium and 59% of body water, respectively, even though they lost no more sodium than those that were alive atpH 3.5 after 1 wk. Toxic effects of low pH involve not only the total amount of body sodium lost but also the rate at which it is lost.

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