Interactions of acid-base status and nitrogen excretion and metabolism in the ureogenic teleost Opsanus beta

Interactions of acid-base status and nitrogen excretion and metabolism in the ureogenic teleost Opsanus beta
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产尿硬骨鱼 Opsanus beta 中酸碱状态与氮排泄和代谢的相互作用

DOI:
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发表时间:
1993
期刊:
影响因子:
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通讯作者:
P. Walsh
P. Walsh
中科院分区:
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文献类型:
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作者:
M. Barber;P. Walsh

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通过将蟾蜍暴露于各种水处理中,研究了海湾蟾蜍 Opsanus beta(一种产尿硬骨鱼)的酸碱状态、废氮排泄和代谢的相互作用。我们的测量表明,与其他海洋硬骨鱼一样,蟾蜍通过操纵血液[HCO3-]快速调节酸碱状态。一些处理影响氮排泄。高碳酸血症的初始阶段(1% CO2)导致尿素生成显着减少,后期补偿阶段(血浆 [HCO3-] 升高)导致尿素生成显着增加。用 HCl 处理水(降低 pH 值并减少碳酸盐含量)可显着抑制尿素生成。随后的 NH4Cl 负载实验和其他几种处理表明,这种抑制不太可能是酸碱扰动的结果,但可能是鱼将废氮以氨的形式排出的能力增强,从而降低了尿素生成的驱动力。酶活性和肝细胞尿生成潜能不受各种酸碱处理的影响,但血浆氨基酸水平的显着降低与高碳酸血症引起的血浆[HCO3-]增加有关。与我们的治疗相关的尿素生成的变化似乎主要是由于底物水平的变化,而不是生化机制的整体变化。我们的结果是在阿特金森及其同事的假设的背景下讨论的,即尿素生成是通过碳酸氢盐消耗进行酸碱调节的一种手段。
The interactions of acid-base status, waste nitrogen excretion and metabolism in the gulf toadfish Opsanus beta, a ureogenic teleost, were examined by exposing toadfish to a variety of water treatments. Our measurements show that, like other marine teleosts, toadfish rapidly regulate acid- base status by manipulating blood [HCO3-]. Several treatments affected nitrogen excretion. The initial stages of hypercapnia (1 % CO2) led to significant reductions in ureogenesis, and the later compensated stages (with elevated plasma [HCO3-]) led to significant increases in ureogenesis. Treatment of water with HCl (which lowered pH and reduced the carbonate content) substantially inhibited ureogenesis. Subsequent experiments with NH4Cl loading and several other treatments suggest that this depression is less likely to be the result of acid-base perturbations, but is probably an enhancement of the fish9s ability to excrete waste nitrogen as ammonia, thereby decreasing the drive for ureogenesis. Enzyme activities and hepatocyte ureogenic potential were unaffected by various acid-base treatments, but a significant depletion of plasma amino acid levels was associated with the increase in plasma [HCO3-] induced by hypercapnia. Changes in ureogenesis associated with our treatments appear to be due primarily to changes in substrate levels, rather than to wholesale changes of the biochemical machinery. Our results are discussed in the context of the hypothesis of Atkinson and colleagues, that ureogenesis is a means for acid-base regulation via bicarbonate consumption.