The effect of dietary protein restriction on the secretory dynamics of 1α-hydroxycorticosterone and urea in the dogfish, Scyliorhinus canicula: a possible role for 1α-hydroxycorticosterone in sodium retention
The putative osmoregulatory role of the unique elasmobranch corticosteroid, 1α-hydroxycorticosterone (1α-OH-B), was investigated using dietary protein restriction as a means of limiting urea biosynthetic ability. Groups of dogfish (Scyliorhinus canicula) were adapted to either a high or a low protein diet (HPD and LPD respectively) and the secretory dynamics of urea and 1α-OH-B were determined following acclimation to normal (100%), 130% and 50% sea water.
In normal sea water, LPD fish showed significantly decreased blood production of urea compared with fish fed a HPD (P <0·05), and the plasma urea concentration required to maintain iso-osmolality was achieved only by a substantial decrease in urea clearance from the plasma. Unlike HPD fish, LPD fish in 130% sea water had no apparent ability to increase plasma urea concentration. An alternative strategy adopted by these animals was the retention of high plasma concentrations of Na+ and Cl−, which increased plasma osmolality and tended to decrease osmotic water loss. Concomitant with the increased ion concentrations, plasma 1α-OH-B concentration was also greatly elevated in LPD fish indicating that the steroid may be acting to minimize Na+ (and Cl−) excretion at osmoregulatory sites such as the rectal gland, kidney and gills.
This and a previous study have also demonstrated that 1α-OH-B concentration is elevated in 50% sea water. Decreases in plasma Na+ concentration are tolerated down to 75% sea water, whereafter Na+ is preferentially retained and further decreases in osmolality are achieved by reductions in plasma urea concentration. Increased 1α-OH-B concentration in 50% sea water corresponds to Na+ retention and regulation around a lower set point.
The results of this study are consistent with a mineralocorticoid role for 1α-OH-B in elasmobranchs, with 1α-OH-B acting preferentially to maintain plasma Na+ concentrations under certain osmotic conditions.