Desiccation of Pyramid Lake, Nevada, has led to continued increases in the lake's alkalinity (currently pH 9.4) that may threaten the resident Lahontan cutthroat trout population. In this study, Lahontan cutthroat trout were challenged with more alkaline water (pH 10). The objectives were to describe physiological responses which may permit survival or lead to death in future potential environmental conditions and to cast further light on the mechanisms of nitrogenous waste excretion, acid-base regulation and ionoregulation in this unusual salmonid. Ammonia excretion (Jamm) was reduced by 50 % in the first few hours, but had fully recovered by 24 h and exceeded control values by 36–48 h. A sustained, twofold elevation of plasma ammonia concentration may have facilitated the recovery of Jamm by increasing the blood-to-water ammonia partial pressure diffusion gradient (deltaPNH3) and NH4+ electrochemical gradient. Urea excretion (Jurea) almost doubled at 24–48 h of pH 10 exposure. Activities of ornithine-urea cycle enzymes in the liver were very low and there was no induction at pH 10. However, all three enzymes of the uricolytic pathway were present, and allantoicase activity increased significantly at pH 10, a possible explanation for the elevated Jurea. Increased liver glutamine synthetase activity at pH 10 is consistent with a possible ammonia detoxification mechanism. A combined respiratory (decreased PaCO2) and metabolic (gain of basic equivalents) alkalosis developed at pH 10 and resulted in a 0.25 unit increase in arterial blood pH. Electrochemical gradients for CO32- and OH- entry and H+ efflux all increased, but the gradient for HCO3- entry decreased to zero. Blood lactate level increased without marked changes in arterial O2 tension, suggesting that increased lactic acid production contributed to acid-base control. Plasma Na+ and Cl- levels decreased and K+ level increased during pH 10 exposure. Survival at pH 10 was relatively poor: more than 50 % of the fish died after 72 h exposure. Greatly elevated plasma PNH3 and depressed plasma Na+ and Cl- levels in non-surviving trout suggest that a combination of ammonia toxicity and ionoregulatory failure led to death in susceptible cutthroat trout.

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