THE EFFECTS OF HYPERCAPNIA ON BRANCHIAL AND RENAL CALCIUM FLUXES IN THE RAINBOW-TROUT (ONCORHYNCHUS-MYKISS)

Citation
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
Citations number
45
Categorie Soggetti
Zoology,Physiology
ISSN journal
01741578
Volume
167
Issue
1
Year of publication
1997
Pages
52 - 60
Database
ISI
SICI code
0174-1578(1997)167:1<52:TEOHOB>2.0.ZU;2-O
Abstract
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.