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.
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.
This study employed a recently developed radioisotopic assay (Wood and Perry 1991) to examine the inhibition, induced by catecholamines, of the conversion of plasma HCO 3 (-) to CO2 in acidotic trout blood, and the influence of oxygenation status on the response. Blood was incubated in vitro at PCO 2= 2 torr, and 10(-6) M noradrenaline was employed as the adrenergic stimulus. In particular we investigated whether the inhibition of plasma HCO 3 (-) conversion could be explained by a limited supply of H(+)s for the intracellular HCO 3 (-) dehydration reaction because of competition by the adrenergically activated Na /H(+) exchanger. Hypoxia (PO 2= 15 torr) was employed as a tool to intensify this competition. Hypoxia raised RBC pHi, pHe, and plasma total CO2 concentration (CCO 2) by the Haldane effect, and increased the magnitude of Na(+)/H(+) activation, expressed as the change in the transmembrane pH gradient (pHe-pHi). However hypoxia did not alter the inhibition of the conversion of plasma HCO 3 (-) to CO2 caused by noradrenaline. Hypoxia itself stimulated the RBC-mediated conversion of plasma HCO 3 (-) to CO2 by about 20% in the presence or absence of noradrenaline. The conversion rate was strongly correlated with pHe, pHe-pHi, and plasma CCO 2 in these experiments, but not with pHi. We conclude that adrenergically mediated inhibition in the conversion of plasma HCO 3 (-) to CO2 by trout RBCs is not due to competitive limitation on intracellular H(+)s, but rather to changes in the electrochemical gradient for HCO 3 (-) entry and/or to CO2 recycling from plasma to RBC. The deoxygenated condition helps to promote CO2 excretion at the level of the RBC.
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