Author(s): Verbost PM, Flik G, Fenwick JC, Greco AM, Pang PK,
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Abstract The branchial Ca(2+) uptake by teleost fish is under inhibitory control by the hormone stanniocalcin (STC) which is generated by the corpuscles of Stannius (CS). Removal of the CS in North American eel, Anguilla rostrata LeSueur, induced a rapid rise in blood calcium levels. Branchial Ca(2+) influx following the extirpation of the CS (stanniectomy, STX) increased during the first four days and stayed elevated thereafter (in agreement with previous studies). The transepithelial potential (TEP) across the gills did not change after STX and this means that the electrochemical gradient for Ca(2+) is less favourable for passive influx of Ca(2+) in STX eel. Therefore, the Ca(2+) influx in STX eels is a transcellular flux, with Ca(2+) crossing the apical and basolateral membrane barrier. The kinetics of ATP-driven Ca(2+)-transport across basolateral plasma membranes from eel gills did not change after STX. Thus, the increased Ca(2+)-influx after STX is not correlated with changes in ATP-dependent Ca(2+)-extrusion across the basolateral membrane, suggesting a regulation at the apical membrane. Moreover, STC did not affect ATP-driven Ca(2+)-transport in isolated basolateral membranes (in vitro). STC (0.1 nM) reduced cAMP levels in dispersed eel gill cells. It had no significant effect on the IP3 levels in these cells. We postulate that STC controls the permeability to Ca(2+) of the apical membranes of the Ca(2+) transporting cells of fish gills by controlling second messenger operated Ca(2+) channels in the apical membrane.
This article was published in Fish Physiol Biochem
and referenced in Journal of Environmental & Analytical Toxicology