Adrenergic Regulation of Blood Acid-Base Status following Exhaustive Exercise in Seawater-Adapted Rainbow Trout, Salmo gairdneri

Abstract

Isoproterenol (β adrenoceptor agonist), propranolol (β adrenoceptor antagonist), or saline (sham) was administered to seawater-adapted rainbow trout immediately after exhaustive exercise in order to assess the role of β-adrenoceptor stimulation in the correction of postexercise blood acid-base disturbances. Exhaustive exercise induced a severe blood acidosis of respiratory and metabolic origin. Recovery from the acidosis was inhibited by β -blockade and facilitated by β-agonist addition. βblockade caused a reduction in branchial H⁺ equivalent excretion to the environmental water and a comparatively large and enduring respiratory acidosis. These likely arose as a result of an inhibition of branchial ion exchanges or through decreases in branchial ventilation, gill blood perfusion, and/or gill membrane permeability. Relative to the control fish, addition of a β-agonist caused no additional change in branchial acid excretion. However, the recovery of blood pH was very rapid, and this eventually led to an over compensation due to a mixed respiratory and metabolic alkalosis. In the absence of any effect on branchial H ⁺ equivalent flux, the metabolic alkalosis induced by the β-agonist could be attributed to a stimulation of H⁺ equivalent exchange between extra- and intracellular compartments. We conclude that β-adrenergic responses play an important role in the regulation of postexercise blood acid-base status in seawater-adapted trout.