Ammonia (NH3 + NH4+) is the major nitrogenous waste in teleost fish. NH3 is also the third respiratory gas, playing a role in ventilatory control. However it is also highly toxic. Normally, ammonia excretion through the gills occurs at about the same rate as its metabolic production, but the branchial transport mechanisms have long been controversial. An influential review in this journal has claimed that ammonia excretion in fish is probably limited by diffusion rather than by convection, so that increases in ventilation would have negligible effect on the rate of ammonia excretion. Why then should elevated plasma ammonia stimulate ventilation? The diffusion-limitation argument was made before the discovery of Rhesus (Rh) glycoproteins and the associated metabolon in the gills, which serve to greatly increase branchial ammonia permeability under conditions of ammonia loading. Therefore, we hypothesized here that (i) in accord with the diffusion-limitation concept, changes in ventilation would not affect the rate of ammonia excretion under conditions where branchial Rh metabolon function would be low (resting trout with low plasma ammonia levels). However, we also hypothesized that (ii) in accord with convective limitation, changes in ventilation would influence the rate of ammonia excretion under conditions where diffusion limitation was removed because branchial Rh metabolon function would be high (ammonia-loaded trout with high plasma ammonia levels). We used variations in environmental O2 levels to manipulate ventilation in trout under control or ammonia-loaded conditions - i.e. hyperventilation in moderate hypoxia or hypoventilation in moderate hyperoxia. In accord with hypothesis (i), under resting conditions, ammonia excretion was insensitive to experimentally induced changes in ventilation. Ammonia-loading by NH4HCO3 infusion for 30h + increased the gill mRNA expressions of two key metabolon components (Rhcg2, V-H+-ATPase or HAT), together with a 7.5-fold increase in plasma ammonia concentration and a 3-fold increase in ammonia excretion rate. In accord with hypothesis (ii), in these fish, hypoxia-induced increases in ventilation elevated the ammonia excretion rate and lowered plasma ammonia, while hyperoxia-induced decreases in ventilation reduced the ammonia excretion rate, and elevated plasma ammonia concentration. We conclude that under conditions of natural ammonia loading (e.g. meal digestion, post-exercise recovery), diffusion-limitation is removed by Rh metabolon upregulation, such that the stimulation of ventilation by elevated plasma ammonia can play an important role in clearing the potentially toxic ammonia load.

中文翻译：

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虹鳟Oncorhynchus mykiss的g通风会影响氨的排泄吗？

氨（NH3 + NH4 +）是硬骨鱼中的主要含氮废物。NH3也是第三种呼吸气体，在呼吸控制中起作用。但是它也是剧毒的。通常，通过the排泄氨的速率与其代谢产生的速率大致相同，但是分支转运机制一直存在争议。该杂志上的一篇有影响力的评论声称，鱼类中氨的排泄可能受扩散而不是对流的限制，因此通风量的增加对氨排泄率的影响可忽略不计。那么为什么血浆氨升高会刺激通气？在发现恒河猴（Rh）糖蛋白和associated中相关的代谢素之前就进行了扩散限制论证，在氨的负载条件下，其可极大地提高分支氨的渗透性。因此，我们在这里假设（i）根据扩散限制的概念，在分支Rh Rh代谢功能较低（血浆氨水平低的静止鳟鱼）的条件下，通风的变化不会影响氨的排泄速率。但是，我们还假设（ii）根据对流限制，在去除扩散限制的条件下，通风的变化会影响氨的排泄速率，因为分支Rh代谢酶功能较高（氨水鳟鱼血浆氨水平较高） ）。我们利用环境中O2含量的变化来控制或控制氨气条件下鳟鱼的通风-即 中度低氧时换气过度或中度高氧时换气不足。根据假设（i），在静止条件下，氨的排泄对实验引起的通风变化不敏感。NH4HCO3输注氨气30h +可增加两个关键代谢物组分（Rhcg2，V-H + -ATPase或HAT）的ill mRNA表达，同时血浆氨浓度增加7.5倍，氨增加3倍排泄率。根据假设（ii），在这些鱼中，低氧引起的通气增加会增加氨的排泄率，降低血浆氨，而高氧引起的通气减少会降低氨的排泄率，并增加血浆氨浓度。我们得出结论，在天然氨负荷的条件下（例如粗粉消化，