PHYSIOLOGICAL ADAPTATIONS OF RAINBOW-TROUT TO CHRONICALLY ELEVATED WATER PH (PH=9.5)

Recent investigations have demonstrated that rainbow trout cope with a cute high pH (pH > 9.0) exposure (lasting 3-8 days) through their abil ity to counteract high-pH-induced disturbances to ammonia excretion (J (Amm)), acid-base homeostasis, and electrolyte balance. In the present investigation our goal was to establish how these physiological proce sses were modulated during chronic (28-day) high pH (pH = 9.5) exposur e. Chronic high pH led to minimal mortality, and there were no long-te rm changes in stress indicators levels, such as cortisol or glucose. J (Amm) was initially reduced by 40% at high pH but rapidly recovered an d fluctuated around control rates, thereafter. Decreased J(Amm) was as sociated with an initial 2.5-fold increase in plasma ammonia concentra tions (T-Amm), followed by a return toward pre-exposure levels after 3 days. Overall, plasma T-Amm was slightly higher (40-80%) in the treat ment fish, and this likely led to plasma PNH3S that were sufficient to sustain J(Amm) at high pH. White muscle T-Amm stores were also chroni cally elevated, by 50-100%. There was a transient, twofold elevation o f J(Urea) immediately following high-pH exposure, but by 3 days J(Urea ) had returned to control rates and stabilized thereafter. Plasma ion balance was well maintained at high pH, despite a chronic depression o f 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 ac id production. White muscle intracellular pH (pH(i)) was unaltered dur ing high pH exposure. We conclude that the long-term survival of rainb ow trout in alkaline environments is facilitated by higher steady-stat e internal ammonia concentrations, the development of a sustained, com pensatory metabolic acidosis which offsets decreased plasma P-CO2, and the effective regulation of plasma electrolyte balance. (C) 1996 Wile y-Liss, Inc.