Abstract
Recent investigations have demonstrated that rainbow trout cope with acute high pH (pH > 9.0) exposure (lasting 3–8 days) through their ability to counteract high-pH-induced disturbances to ammonia excretion (JAmm), acid-base homeostasis, and electrolyte balance. In the present investigation our goal was to establish how these physiological processes were modulated during chronic (28-day) high pH (pH = 9.5) exposure. Chronic high pH led to minimal mortality, and there were no long-term changes in stress indicators levels, such as cortisol or glucose. JAmm was initially reduced by 40% at high pH but rapidly recovered and fluctuated around control rates, thereafter. Decreased JAmm was associated with an initial 2.5-fold increase in plasma ammonin concentrations (TAmm), followed by a return toward pre-exposure levels after 3 days. Overall, plasma TAmm was slightly higher (40–80%) in the treatment fish, and this likely led to plasma PNH3s that were sufficient to sustain JAmm at high pH. White muscle TAmm stores were also chronically elevated, by 50–100%. There was a transient, twofold elevation of JUrea immediately following high-pH exposure, but by 3 days JUrea had returned to control rates and stabilized thereafter. Plasma ion balance was well maintained at high pH, despite a chronic depression of Na+ influx. Even though there was a persistent respiratory alkalosis at alkaline pH, blood pH was effectively regulated by a simultaneous metabolic acid load, which was not associated with increased lactic acid production. White muscle intracellular pH (pHi) was unaltered during high pH exposure. We conclude that the long-term survival of rainbow trout in alkaline environments is facilitated by higher steady-state internal ammonia concentrations, the development of a sustained, compensatory metabolic acidosis which offsets decreased plasma PCO2, and the effective regulation of plasma electrolyte balance. © 1996 Wiley-Liss, Inc.
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