Calcium uptake in freshwater rainbow trout (Salmogairdnert) under control conditions (external [Ca2+] ≃ 1·8mequivl−1, [NaCl] ≃ 0·8mequiv 1−1) occurred at approximately equal rates (12–15 equiv 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 in an isolated, saline-perfused head preparation was equal to that in vivo. The cells involved in are mainly located on lamellae rather than on filaments since ∼ 95 % of occurred across the arterio-arterial circulation of the gill. in vitro, displayed Michaelis-Menten kinetics. Acclimation to low external [Ca2+] (50μequivl−1; unchanged [NaCl]) for 1 day caused a five-fold stimulation of characterized by decreased Km and increased Jmax Longer periods of low [Ca2+] acclimation resulted in changes of Jmax only. Jmax 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 Jmax. Fish exposed to high external [Ca2+] (10 μequiv 1−1; unchanged [NaCl]) displayed reduced Similar changes in 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 and elevated plasma [cortisol] in low-[Ca2+] acclimated fish.

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