Kinetics of branchial calcium uptake in the rainbow trout: Effects of acclimation to various external calcium levels

S. F. Perry, C. M. Wood

Research output: Contribution to journalArticle

194 Citations (Scopus)

Abstract

Calcium uptake (J(in)(Ca)) in freshwater rainbow trout (Salmo gairdneri) under control conditions (external [Ca2+] ≃ 1.8 mequiv l-1, [NaCl] ≃ 0.8 mequiv l-1) occurred at approximately equal rates (12-15 μequiv kg-1 h-1) through the gills and the general body surface in vivo. The gut was not involved. Under the same conditions, in vitro branchial J(in)(Ca) in an isolated, saline-perfused head preparation was equal to that in vivo. The cells involved in J(in)(Ca) are mainly located on lamellae rather than on filaments since ~95% of J(in)(Ca) occurred across the arterio-arterial circulation of the gill. J(in)(Ca), in vitro, displayed Michaelis-Menten kinetics. Acclimation to low external [Ca2+] (50 μequiv l-1; unchanged [NaCl]) for 1 day caused a five-fold stimulation of J(in)(Ca) characterized by decreased K(m) and increased J(max). Longer periods of low [Ca2+] acclimation resulted in changes of J(max) only. J(max) gradually returned towards control levels as acclimation time increased, but was still elevated after 30 days. Acclimation to low ambient [Ca2+] caused proliferation and increased exposure of lamellar chloride cells which were correlated with increased J(max). Fish exposed to high external [Ca2+] (10 mequiv l-1; unchanged [NaCl]) displayed reduced J(in)(Ca). Similar changes in J(in)(Ca) were observed during in vivo experiments. Plasma Ca2+ concentration remained constant regardless of external [Ca2+], while plasma Na+ and Cl- levels were transiently reduced at 1 day low [Ca2+] exposure but had recovered by 7 days. A possible role for cortisol in Ca2+ regulation is discussed based on observations of cortisol-stimulated lamellar chloride cell proliferation and J(in)(Ca), and elevated plasma [cortisol] in low-[Ca2+] acclimated fish.

Original languageEnglish
Pages (from-to)411-433
Number of pages23
JournalJournal of Experimental Biology
VolumeVOL. 116
StatePublished - Dec 1 1985

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Oncorhynchus mykiss
Acclimatization
acclimation
rainbow
calcium
Calcium
uptake mechanisms
Hydrocortisone
kinetics
plasma
Chlorides
Fishes
chloride
fish
sodium chloride
Fresh Water
cortisol
Head
Cell Proliferation
fold

ASJC Scopus subject areas

  • Agricultural and Biological Sciences(all)
  • Agricultural and Biological Sciences (miscellaneous)

Cite this

Kinetics of branchial calcium uptake in the rainbow trout : Effects of acclimation to various external calcium levels. / Perry, S. F.; Wood, C. M.

In: Journal of Experimental Biology, Vol. VOL. 116, 01.12.1985, p. 411-433.

Research output: Contribution to journalArticle

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abstract = "Calcium uptake (J(in)(Ca)) in freshwater rainbow trout (Salmo gairdneri) under control conditions (external [Ca2+] ≃ 1.8 mequiv l-1, [NaCl] ≃ 0.8 mequiv l-1) occurred at approximately equal rates (12-15 μequiv kg-1 h-1) through the gills and the general body surface in vivo. The gut was not involved. Under the same conditions, in vitro branchial J(in)(Ca) in an isolated, saline-perfused head preparation was equal to that in vivo. The cells involved in J(in)(Ca) are mainly located on lamellae rather than on filaments since ~95{\%} of J(in)(Ca) occurred across the arterio-arterial circulation of the gill. J(in)(Ca), in vitro, displayed Michaelis-Menten kinetics. Acclimation to low external [Ca2+] (50 μequiv l-1; unchanged [NaCl]) for 1 day caused a five-fold stimulation of J(in)(Ca) characterized by decreased K(m) and increased J(max). Longer periods of low [Ca2+] acclimation resulted in changes of J(max) only. J(max) gradually returned towards control levels as acclimation time increased, but was still elevated after 30 days. Acclimation to low ambient [Ca2+] caused proliferation and increased exposure of lamellar chloride cells which were correlated with increased J(max). Fish exposed to high external [Ca2+] (10 mequiv l-1; unchanged [NaCl]) displayed reduced J(in)(Ca). Similar changes in J(in)(Ca) were observed during in vivo experiments. Plasma Ca2+ concentration remained constant regardless of external [Ca2+], while plasma Na+ and Cl- levels were transiently reduced at 1 day low [Ca2+] exposure but had recovered by 7 days. A possible role for cortisol in Ca2+ regulation is discussed based on observations of cortisol-stimulated lamellar chloride cell proliferation and J(in)(Ca), and elevated plasma [cortisol] in low-[Ca2+] acclimated fish.",
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N2 - Calcium uptake (J(in)(Ca)) in freshwater rainbow trout (Salmo gairdneri) under control conditions (external [Ca2+] ≃ 1.8 mequiv l-1, [NaCl] ≃ 0.8 mequiv l-1) occurred at approximately equal rates (12-15 μequiv kg-1 h-1) through the gills and the general body surface in vivo. The gut was not involved. Under the same conditions, in vitro branchial J(in)(Ca) in an isolated, saline-perfused head preparation was equal to that in vivo. The cells involved in J(in)(Ca) are mainly located on lamellae rather than on filaments since ~95% of J(in)(Ca) occurred across the arterio-arterial circulation of the gill. J(in)(Ca), in vitro, displayed Michaelis-Menten kinetics. Acclimation to low external [Ca2+] (50 μequiv l-1; unchanged [NaCl]) for 1 day caused a five-fold stimulation of J(in)(Ca) characterized by decreased K(m) and increased J(max). Longer periods of low [Ca2+] acclimation resulted in changes of J(max) only. J(max) gradually returned towards control levels as acclimation time increased, but was still elevated after 30 days. Acclimation to low ambient [Ca2+] caused proliferation and increased exposure of lamellar chloride cells which were correlated with increased J(max). Fish exposed to high external [Ca2+] (10 mequiv l-1; unchanged [NaCl]) displayed reduced J(in)(Ca). Similar changes in J(in)(Ca) were observed during in vivo experiments. Plasma Ca2+ concentration remained constant regardless of external [Ca2+], while plasma Na+ and Cl- levels were transiently reduced at 1 day low [Ca2+] exposure but had recovered by 7 days. A possible role for cortisol in Ca2+ regulation is discussed based on observations of cortisol-stimulated lamellar chloride cell proliferation and J(in)(Ca), and elevated plasma [cortisol] in low-[Ca2+] acclimated fish.

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