Erratum

1986 ◽  
Vol 123 (1) ◽  
pp. 216-216
Author(s):  
S. F. PERRY ◽  
C. M. WOOD

Kinetics of branchial calcium uptake in the rainbow trout: effects of acclimation to various external calcium levels. J. exp. Biol. 116, 411–433.

1985 ◽  
Vol 116 (1) ◽  
pp. 411-433 ◽  
Author(s):  
S. F. PERRY ◽  
C. M. WOOD

Calcium uptake (JCain) in freshwater rainbow trout (Salmo gairdnen) under control conditions (external [Ca2+] ≃ 1.8 mequivl−1, [NaCl] ≃ 0.8 mequiv 1−1) 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 JCain in an isolated, saline-perfused head preparation was equal to that in vivo. The cells involved in JinCa are mainly located on lamellae rather than on filaments since 95 % of JinCa occurred across the arterio-arterial circulation of the gill. JinCa, in vitro, displayed Michaelis-Menten kinetics. Acclimation to low external [Ca2+] (50 μequiv 1−1; unchanged [NaCl]) for 1 day caused a five-fold stimulation of JinCa characterized by decreased Km and increased J max. 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 mequivl−1; unchanged [NaCl]) displayed reduced JinCa Similar changes in JinCa 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 JinCa, and elevated plasma [cortisol] in low-[Ca2+] acclimated fish.


1994 ◽  
Vol 186 (1) ◽  
pp. 55-73 ◽  
Author(s):  
C. Hogstrand ◽  
R. W. Wilson ◽  
D. Polgar ◽  
C. M. Wood

The effects of sublethal waterborne Zn2+ (150 micrograms l-1 = 2.3 mumol-1) on the kinetics of unidirectional Ca2+ influx were studied in juvenile freshwater rainbow trout during chronic exposure (60 days) at a water [Ca2+] of 1.0 mmol l-1. An unexposed group held under identical conditions served as control. The presence of Zn2+ in the water increased the apparent Km for Ca2+ influx by up to 300% with only a small inhibitory effect (35% at most) on the maximum rate of uptake (Jmax). These results, in combination with earlier data showing that Ca2+ competitively inhibits Zn2+ uptake, suggest that Zn2+ and Ca2+ compete for the same uptake sites. Acute withdrawal of Zn2+ after 3h of exposure resulted in a 23-fold reduction in Km for Ca2+, but a persistent small depression of Jmax. During prolonged exposure to Zn2+, the apparent Km for Ca2+ remained greatly elevated and Jmax remained slightly depressed. The actual Ca2+ influx in hard water ([Ca2+] = 1.0 mmol l-1) decreased marginally and paralleled the small changes in Jmax. The increases in apparent Km had a negligible influence on the actual Ca2+ influx because Km values (38–230 mumol l-1), even when elevated by Zn2+, remained below the water [Ca2+] (1000 mumol l-1). Rainbow trout exposed to Zn2+ exhibited a slower rate of protein synthesis in the gills (measured on day 23) and an increased tolerance to Zn2+ challenge (measured on both days 27 and 50). Unidirectional Zn2+ influx, measured at the end of the exposure period, was significantly reduced in the Zn2+-exposed fish. There were no changes in hepatic or branchial Zn2+, Cu2+ or metallothionein concentrations. We hypothesize that, during exposure to sublethal [Zn2+] in hard water, the fish may change the Km for a mutual Ca2+/Zn2+ carrier so as to reduce markedly Zn2+ influx without greatly altering Ca2+ influx. This reduced Zn2+ influx, rather than metallothionein induction, may be the basis of adaptation to elevated concentrations of waterborne Zn2+.


Biochemistry ◽  
1983 ◽  
Vol 22 (23) ◽  
pp. 5254-5261 ◽  
Author(s):  
Dorothy H. Pierce ◽  
Antonio Scarpa ◽  
Michael R. Topp ◽  
J. Kent Blasie

1988 ◽  
Vol 254 (6) ◽  
pp. R891-R896 ◽  
Author(s):  
F. P. Lafeber ◽  
G. Flik ◽  
S. E. Wendelaar Bonga ◽  
S. F. Perry

Bidirectional whole body flux and branchial Ca2+ influx were measured in freshwater rainbow trout. Intra-arterial injections of homogenates of Stannius corpuscles (CS) as well as of a 54-kDa isolated product (hypocalcin) exerted an inhibitory effect on whole body Ca2+ influx, but did not effect Ca2+ efflux. Hypocalcin was more effective in reducing Ca2+ influx in trout acclimated to low-calcium freshwater than in fish from normal-calcium water. We conclude that the isolated product (hypocalcin) represents the hypocalcemic principle of the CS. Similar doses of hypocalcin caused quantitatively similar decreases in Ca2+ influx in vivo and in the isolated perfused head preparation. This indicates that the gills form the principle target for hypocalcin in trout. The branchial transepithelial potential did not change during hormone treatments. Possible mechanisms of hypocalcin action are suggested.


1975 ◽  
Vol 30 (11-12) ◽  
pp. 777-780 ◽  
Author(s):  
Pierre Ermier ◽  
Wilhelm Hasselbach

Abstract The amplitude of the fast uptake and the initial rate of the slow uptake increase with in­ creasing free calcium concentrations, up to 30 μᴍ. In that range, both processes are correlated to each other. At higher concentrations, the slow uptake is more inhibited than the fast uptake. The fast uptake shows a maximum amplitude which remains unchanged in the presence of phosphate. The slow uptake leads to a nearly complete depletion of the external calcium, and its rate is proportional to the phosphate concentration, even at physiological range. The sarcoplasmic ATPase liberates inorganic phosphate and the slow uptake


1985 ◽  
Vol 40 (7-8) ◽  
pp. 571-575 ◽  
Author(s):  
Wilhelm Hasselbach ◽  
Andrea Migala

Abstract The decline of the transport ratio of the sarcoplasmic calcium pump observed in a recent study (A. results from the retardation of calcium oxalate precipitation at low calcium/protein ratios. The prevailing high internal calcium level supports a rapid calcium backflux and a compensatory ATP hydrolysis during net calcium uptake which reduces the transport ratio. Yet, the determined calcium back­ flux does not fully account for the decline of the transport ratio. A supposed modulation of the stoichiometry of the pump by external calcium (0.1 μм) is at variance with results of previous studies showing a constant transport ratio of two in the same calcium concentration range.


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