Abstract
Salmonids experience severe disturbances in the excretion and internal regulation of ammonia, acid-base balance, and ionoregulation when challenged with alkaline pH. We followed the responses of a high-pH-tolerant salmonid, the Lahontan cutthroat trout (Oncorhynchus clarki henshawi) for 72 h after transfer from pH 8. 4 well water into the alkaline water (pH 9. 4) of Pyramid Lake, Nevada. Fish that had been living in Pyramid Lake for 3 wk, 5 wk, and 2 yr were also examined. A combined metabolic and respiratory alkalosis (negative metabolic acid load and decreased arterial CO₂ tension [Paco₂], respectively) occurred initially. The metabolic component was corrected within 24 h, but the respiratory component persisted for up to 5 wk. Transfers also resulted in an immediate 70% reduction in the ammonia excretion rate (JAmm) and a 30% increase in total plasma ammonia TAmm. The TAmm was corrected within 3 d, but JAmm remained depressed, which indicates reduced ammonia production rates. Because the urea excretion rate (JUrea) did not change, the contribution of JUrea to total N excretion increased from 10% in well water to 25% in fish acutely and chronically exposed to lake water. Liver enzyme activities indicated that the pathway for urea production was uricolysis, not the ornithine-urea cycle. Branchial chloride cell fractional surface area increased in lake water, and this may have counteracted the base load by promoting base equivalent excretion via Cl⁻/HCO₃⁻ exchange. Plasma Na⁺ and Cl⁻ levels were slightly higher in Pyramid Lake water. We conclude that the Lahontan cutthroat trout are able to survive in Pyramid Lake's alkaline environment because of their ability to reduce ammonia production, thereby avoiding chronic elevation of plasma TAmm and their ability to control blood acid-base and ionic status under alkaline conditions.
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