Effects of prolactin and growth hormone on strategies of hypoosmotic adaptation in a marine teleost, Sparus sarba.

Silver seabream (Sparus sarba) held in seawater (33 per thousand) or acclimated to a hypoosmotic environment of 6 per thousand were given intraperitoneal injections of saline (0.8% NaCl), recombinant bream growth hormone (rbGH, 1 microg/g), or ovine prolactin (oPRL, 6microg/g) for 7 consecutive days. Serum Na+ levels were unaffected by hypoosmotic acclimation and rbGH and oPRL treatment. Treatment of seawater fish with oPRL resulted in hyperchloremia. In 6 per thousand, saline-treated fish exhibited elevated branchial chloride cell (CC) numbers and exposure indices, all of which were markedly reduced by oPRL. CC numbers and morphometrics were unaffected by oPRL in seawater fish. In contrast, rbGH treatment of seawater fish resulted in elevated CC numbers, apical area, and fractional area and, in 6 per thousand fish, elevated CC fractional area and exposure numbers. Branchial Na+-K+-ATPase activity reduced in saline-treated fish adapted to 6% but was unaffected by rbGH regardless of salinity. oPRL reduced activity in both seawater and 6 per thousand-adapted fish. Neither hypoosmotic adaptation nor oPRL had any effect on renal Na+-K+-ATPase activity whereas rbGH reduced activity in both 33 and 6 per thousand. Saline-treated fish adapted to 6 per thousand exhibited reduced Na+-K+-ATPase activity in most regions of the intestine. Treatment with rbGH did not change intestinal Na+-K+-ATPase activity of seawater fish but elevated activity in the anterior regions (esophagus and stomach) of 6 per thousand-adapted fish. Treatment with oPRL elevated Na+-K+-ATPase activity throughout the gastrointestinal tract of seawater fish and in the anterior reaches of 6 per thousand-adapted fish. The data indicated that the as yet uncharacterized osmoregulatory roles of PRL and GH in seabream may warrant further attention as the present study connoted differing responses to that of other teleosts studied. Copyright 1999 Academic Press.