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Rainbow trout were infused continuously for 24 h with epinephrine in order to elevate circulating levels of this hormone to those measured during periods of acute extracellular acidosis (approximately 5 X 10(-8) mol l-1). Concomitant effects on selected blood respiratory acid-base and ionic variables were evaluated. Infusion of epinephrine caused a transient respiratory acidosis as a result of hypoventilation and/or inhibition of red blood cell (RBC) bicarbonate dehydration. The acidosis was regulated by gradual accumulation of plasma bicarbonate. Even though whole blood pH (pHe) was depressed by 0.16 units, RBC pH (pHi) remained constant, thereby causing the transmembrane pH gradient (pHe-pHi) to decrease. A similar effect of epinephrine on RBC pH was observed in vitro, although the response required a higher concentration of epinephrine (2.0 X 10(-7) mol l-1). We speculate that the release of epinephrine during periods of depressed blood pH is important for preventing excessive shifts in RBC pH and for initiating a series of responses leading to plasma HCO3- accumulation and eventual restoration of blood acid-base status.

Acute exposure of rainbow trout (Salmo gairdneri) to low external calcium (25 microM) caused an immediate but transient increase in plasma epinephrine concentration that may have been related to a concomitant depression of blood pH. Intra-arterial infusion of epinephrine at normal ambient calcium levels (0.35 mM) for 4 h caused circulating levels of epinephrine to rise from 2.9 X 10(-9) to 8.0 X 10(-8) M but did not affect norepinephrine levels, or branchial unidirectional calcium fluxes. Active (ATP-dependent) calcium transport across basolateral plasma membranes prepared from gill epithelial cells was not affected by pretreatment of fish with epinephrine or by direct application of epinephrine or cAMP, in vitro. Epinephrine infusion elevated urine flow rate, decreased urine pH, and increased urine phosphate levels significantly. Net renal calcium efflux increased significantly as a result of the increased urine flow rate. It is concluded that epinephrine does not stimulate branchial calcium uptake or renal conservation of calcium in rainbow trout at normal external calcium levels and therefore we cautiously suggest that epinephrine is unlikely to be involved in calcium balance during periods of exposure to low external calcium. Instead, epinephrine may play a role in compensating the acid-base disturbances and the increased branchial water influx that are associated with exposure to low ambient calcium.

Rainbow trout were infused continuously for 24 h with epinephrine in order to evaluate the effects of elevated circulating levels of epinephrine on selected renal variables. Pronounced effects of epinephrine included elevation of urine flow rate and concomitant increases in the excretion of all measured electrolytes (Na+, Cl-, K+, Ca2+, inorganic phosphate) with the exception of ammonium and bicarbonate ions. Significant reductions in the tubular reabsorption of Na+ and Cl- also contributed to enhanced excretion of these ions. Similarly, epinephrine affected the tubular handling of NH4+ and HCO3- with NH4+ secretion decreasing and HCO3- reabsorption increasing. We speculate that the stimulation of HCO3- reabsorption was a consequence of elevated tubular H+ secretion. Such a mechanism may be important to permit plasma HCO3- retention during periods of internal acidosis. The results are discussed with reference to the role of the fish kidney in regulating acid-base disturbances and the possible interactive effects of elevated epinephrine.

Rainbow trout were infused continuously for 24 h with epinephrine in order to elevate circulating levels to those measured during periods of acute extracellular acidosis (about 5 X 10(-8) mol l-1). Concomitant effects on branchial solute fluxes were evaluated. Epinephrine infusion caused complex and differential adjustments of Na+ and Cl- unidirectional fluxes (influx and efflux) resulting in a significant elevation of the arithmetic difference between Na+ and Cl- net fluxes (JnetNa+-JnetCl-). A significant correlation existed between JnetNa+-JnetCl- and net branchial acid excretion (JnetH+), thereby suggesting a role for epinephrine in piscine acid-base regulation. The stimulation of JnetH+ by epinephrine was due primarily to a reduction in the excretion of titratable acid (JTA) accompanied by non-significant changes in ammonia excretion (JAmm). The results are discussed with respect to a role for epinephrine in regulating acid-base disturbances by interacting with branchial ionic exchange mechanisms.