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A marine teleost,Opsanus beta, compensates acidosis in hypersaline water by H(+)excretion or reduced HCO(3)(-)excretion rather than HCO(3)(-)uptake

文献类型： 外文期刊

作者： Yao, Zongli 1 ; Schauer, Kevin L. 2 ; Ruhr, Ilan M. 2 ; Mager, Edward M. 2 ; Heuer, Rachael M. 2 ; Grosell, Martin 1 ;

作者机构： 1.Chinese Acad Fisheries Sci, East China Sea Fisheries Res Inst, Sino US Joint Lab Aquat Anim Physiol, Shanghai, Peoples R China

2.Univ Miami, Rosenstiel Sch Marine & Atmospher Sci, Dept Marine Biol & Ecol, 4600 Rickenbacker Causeway, Miami, FL 33149 USA

3.Univ North Texas, Dept Biol Sci, Denton, TX 76203 USA

4.Univ Manchester, Sch Med Sci, Cardiovasc Sci, Manchester, Lancs, England

关键词： H(+)excretion; H+-ATPase; Osmoregulation; Metabolic acidosis; Hypersaline water

期刊名称：JOURNAL OF COMPARATIVE PHYSIOLOGY B-BIOCHEMICAL SYSTEMS AND ENVIRONMENTAL PHYSIOLOGY （ 影响因子：2.2； 五年影响因子：2.605 ）

ISSN： 0174-1578

年卷期：

页码：

收录情况： SCI

摘要： Increases in ambient salinity demand parallel increases in intestinal base secretion for maintenance of osmoregulatory status, which is likely the cause of a transient acidosis following transfer of euryhaline fish from freshwater to seawater. It was predicted that transfer of the marine Gulf toadfish (Opsanus beta) from seawater (35 ppt) to hypersaline (60 ppt) seawater (HSW) would lead to a transient acidosis that would be compensated by increases in branchial acid excretion to offset the acid-base disturbance. Toadfish exposed to HSW showed a significant decrease in blood pH and [HCO3-] but no increase in pCO(2), followed by a full recovery after 48-96 h. A similar metabolic acidosis and recovery was found when fish were exposed to 60-ppt HCO3--free seawater (HEPES-buffered), which may suggest that compensation for intestinal base loss during hypersaline treatment is from gill H(+)excretion rather than gill HCO(3)(-)uptake. However, we cannot rule out that reduced branchial HCO(3)(-)excretion contributed to an increase in net acid excretion. Since colchicine prevents full compensation, translocation of H(+)and/or HCO(3)(-)transporters between cytosolic compartments and plasma membrane fractions might be involved in compensating for the hypersalinity-induced acidosis. Translocation of transporters rather than de novo synthesis may represent a faster and less energetically demanding response to rapidly fluctuating and high salinities encountered by toadfish in their natural environment.

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