Department of Biology, University of Ottawa, 30 Marie Curie, Ottawa, ON, K1N 6N5, Canada.
J Comp Physiol B. 2011 May;181(4):501-15. doi: 10.1007/s00360-010-0540-4. Epub 2010 Dec 7.
Fish compensate for acid-base disturbances primarily by modulating the branchial excretion of acid-base equivalents, with a supporting role played by adjustment of urinary acid excretion. The present study used metabolic acid-base disturbances in rainbow trout, Oncorhynchus mykiss, to evaluate the role played by cortisol in stimulating compensatory responses. Trout infused with acid (an iso-osmotic solution of 70 mmol L(-1) HCl), base (140 mmol L(-1) NaHCO(3)) or saline (140 mmol L(-1) NaCl) for 24 h exhibited significant elevation of circulating cortisol concentrations. Acid infusion significantly increased both branchial (by 328 μmol kg(-1) h(-1)) and urinary (by 5.9 μmol kg(-1) h(-1)) net acid excretion, compensatory responses that were eliminated by pre-treatment of trout with the cortisol synthesis inhibitor metyrapone (2-methyl-1,2-di-3-pyridyl-1-propanone). The significant decrease in net acid excretion (equivalent to enhanced base excretion) of 203 μmol kg(-1) h(-1) detected in base-infused trout was unaffected by metyrapone treatment. Acid- and base-infusions also were associated with significant changes in the relative mRNA expression of branchial and renal cytosolic carbonic anhydrase (tCAc) and renal membrane-linked CA IV (tCA IV). Cortisol treatment caused changes in CA gene expression that tended to parallel those observed with acid but not base infusion. For example, significant increases in renal relative tCA IV mRNA expression were detected in both acid-infused (2x) and cortisol-treated (10x) trout, whereas tCA IV mRNA expression was significantly reduced (~5x) in base-infused fish. Despite changes in CA gene expression in acid- or base-infused fish, neither acid nor base infusion affected CAc protein levels in the gill, but both caused significant increases in branchial CA activity. Cortisol treatment similarly increased branchial CA activity in the absence of an effect on branchial CAc protein expression. Taken together, these findings provide support for the hypothesis that in rainbow trout, cortisol is involved in mediating acid-base compensatory responses to a metabolic acidosis, and that cortisol exerts its effects at least in part through modulation of CA.
鱼类主要通过调节鳃部酸碱当量的排泄来代偿酸碱失衡，同时尿液酸排泄也起到辅助作用。本研究采用虹鳟代谢性酸碱失衡模型，评估皮质醇在刺激代偿反应中的作用。向虹鳟输注酸（70mmol/L HCl 的等渗溶液）、碱（140mmol/L NaHCO3）或生理盐水（140mmol/L NaCl）24 小时后，鱼血液中皮质醇浓度显著升高。酸输注显著增加了鳃部（328μmol/kg·h）和尿液（5.9μmol/kg·h）的净酸排泄，这些代偿反应在鱼预先用皮质醇合成抑制剂甲吡酮（2-甲基-1,2-二吡啶-1-丙烷酮）处理后被消除。在碱输注的鱼中，净酸排泄（相当于增强的碱排泄）显著下降 203μmol/kg·h，这种下降不受甲吡酮处理的影响。酸和碱输注还与鳃和肾细胞质碳酸酐酶（tCAc）和肾膜结合 CA IV（tCA IV）的相对 mRNA 表达的显著变化相关。皮质醇处理引起 CA 基因表达的变化，这些变化往往与酸输注而不是碱输注观察到的变化相似。例如，在酸输注的鱼（约 2 倍）和皮质醇处理的鱼（约 10 倍）中均检测到肾相对 tCA IV mRNA 表达显著增加，而在碱输注的鱼中 tCA IV mRNA 表达显著降低（约 5 倍）。尽管在酸或碱输注的鱼中 CA 基因表达发生变化，但酸或碱输注均未影响鳃中的 CAc 蛋白水平，但均导致鳃 CA 活性显著增加。皮质醇处理同样增加了无鳃 CAc 蛋白表达变化的鳃 CA 活性。总之，这些发现为以下假说提供了支持：在虹鳟中，皮质醇参与介导对代谢性酸中毒的酸碱代偿反应，皮质醇的作用至少部分通过调节 CA 来发挥。
