BRANCHIAL CALCIUM-UPTAKE - POSSIBLE MECHANISMS OF CONTROL BY STANNIOCALCIN

The branchial Ca2+ uptake by teleost fish is under inhibitory control by the hormone stanniocalcine (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 Ca2+ 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 Ca2+ is less favourable for passive influx of Ca2+ in STX eel. Therefore, the Call influx in STX eels is a transcellular flux, with Ca2+ crossing the apical and basolateral membrane barrier. The kinetics of ATP-driven Ca2+-transport across basolateral plasma membranes from eel gills did not change after STX. Thus, the increased Ca2+-influx after STX is not correlated with changes in ATP-dependent Ca2+-extrusion across the basolateral membrane, suggesting a regulation at the apical membrane. Moreover, STC did not affect ATP-driven Ca2+-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 Ca2+ of the apical membranes of the Ca2 + transporting cells of fish gills by controlling second messenger operated Ca2+ channels in the apical membrane.