Physiological characterisation of a pH- and calcium-dependent sodium uptake mechanism in the freshwater crustacean,Daphnia magna

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Abstract
Daphnia are highly sensitive to sodium metabolism disruption caused by aquatic acidification and ionoregulatory toxicants, due to their finely balanced ion homeostasis. Nine different water chemistries of varying pH (4, 6 and 8) and calcium concentration (0, 0.5 and 1 mmol l–1) were used to delineate the mechanism of sodium influx in Daphnia magna. Lowering water pH severely inhibited sodium influx when calcium concentration was high, but transport kinetic analysis revealed a stimulated sodium influx capacity (Jmax) when calcium was absent. At low pH increasing water calcium levels decreased Jmax and raised Km (decreased sodium influx affinity), while at high pH the opposite pattern was observed (elevated Jmax and reduced Km). These effects on sodium influx were mirrored by changes in whole body sodium levels. Further examination of the effect of calcium on sodium influx showed a severe inhibition of sodium uptake by 100 μmol l–1 calcium gluconate at both low (50 μmol l–1) and high (1000 μmol l–1) sodium concentrations. At high sodium concentrations, stimulated sodium influx was noted with elevated calcium levels. These results, in addition to data showing amiloride inhibition of sodium influx (Ki=180 μmol l–1), suggest a mechanism of sodium influx in Daphnia magna that involves the electrogenic 2Na+/1H+ exchanger.

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