The effects of hypercapnia on branchial and renal calcium fluxes in the rainbow trout ( Oncorhynchus mykiss )

Abstract

Whole body calcium influx, branchial calcium efflux, and renal Ca2+ excretion were measured in rainbow trout (Oncorhynchus mykiss) exposed to hypercapnia. These experiments were performed to assess the potential impact on Ca2+ balance of the changes in gill morphology known to accompany respiratory acidosis in this species. After 48 h of hypercapnia, gill filamental chloride cell fractional area was significantly reduced. Despite this reduction and the presumed involvement of the chloride cell in calcium influx, whole body calcium influx was increased after 12 h of hypercapnia and remained elevated for 48 h. Branchial calcium efflux was unaltered during hypercapnia exposure, whereas renal Ca2+ excretion was elevated over preflux values only at 6 h of hypercapnia. Measurement of the kinetics of whole body calcium influx after 48 h of hypercapnia revealed a significant increase in the maximal uptake rate of Ca2+, yet the affinity constant of Ca2+ uptake was unaffected. Measurements of high-affinity Ca2+ -ATPase activities and ATP-dependent Ca2+ transport of gill basolateral membrane vesicles revealed that the ATP-dependent Ca2+ extrusion mechanism of the gills was not affected by hypercapnia. The results of the present study clearly show that the reduced chloride cell surface area that accompanies hypercapnia in trout does not impair calcium homeostasis. Although adjustments to the basolateral membrane high affinity Ca2+ transporter do not appear to play a role, the mechanism(s) underlying the maintenance of calcium homeostasis under hypercapnic conditions are unresolved.