Wm. Mackenzie et Sf. Perry, THE EFFECTS OF HYPERCAPNIA ON BRANCHIAL AND RENAL CALCIUM FLUXES IN THE RAINBOW-TROUT (ONCORHYNCHUS-MYKISS), Journal of comparative physiology. B, Biochemical, systemic, and environmental physiology, 167(1), 1997, pp. 52-60
Whole body calcium influx, branchial calcium efflux, and renal Ca2+ ex
cretion were measured in rainbow trout (Oncorhynchus mykiss) exposed t
o hypercapnia. These experiments were performed to assess the potentia
l impact on Ca2+ balance of the changes in gill morphology known to ac
company respiratory acidosis in this species. After 48 h of hypercapni
a, gill filamental chloride cell fractional area was significantly red
uced. Despite this reduction and the presumed involvement of the chlor
ide cell in calcium influx, whole body calcium influx was increased af
ter 12 h of hypercapnia and remained elevated for 48 h. Branchial calc
ium efflux was unaltered during hypercapnia exposure, whereas renal Ca
2+ excretion was elevated over preflux values only at 6 h of hypercapn
ia. 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-depend
ent Ca2+ transport of gill basolateral membrane vesicles revealed that
the ATP-dependent Ca2+ extrusion mechanism of the gills was not affec
ted by hypercapnia. The results of the present study clearly show that
the reduced chloride cell surface area that accompanies hypercapnia i
n trout does not impair calcium homeostasis. Although adjustments to t
he basolateral membrane high affinity Ca2+ transporter do not appear t
o play a role, the mechanism(s) underlying the maintenance of calcium
homeostasis under hypercapnic conditions are unresolved.