Role of adrenergic-dependent H+ release from red cells in acidosis induced by hypoxia in trout.

The response to severe hypoxia is characterized in trout by a sudden drop in blood pH, which is of metabolic origin, and by an increase in the blood concentration of adrenaline. This acidification is biphasic in nature. The first phase of acidification is not associated with a rise in the blood lactate concentration and no longer occurs after pretreatment of the fish with a beta-blocker agent, propranolol. Thus an acid other than lactic acid is released into the blood at the onset of hypoxia and this release, which is under beta-adrenergic control, is responsible for the first phase of acidification. On the other hand the second phase of acidification is related to an increase in blood lactate and is not modified by a beta-blocker agent. We have also demonstrated that deep hypoxia promotes a rapid increase in red blood cell volume and that this cell enlargement is coincident with a large net uptake of Na+ and Cl-. In the presence of beta-blocking agents the Na+ uptake is blocked and the swelling of the cells is considerably inhibited. The residual swelling is clearly due to the chloride shift induced by both deoxygenation of hemoglobin and change in blood pH. In the light of data obtained in vitro on the effect of catecholamines on trout erythrocytes, it can be considered that the first phase of acidification occurring at the onset of hypoxia, and that is under beta-adrenergic control, is due essentially to the release of H+ by red blood cells in exchange with external sodium mediated by a beta-adrenergic-stimulated Na+-H+ exchanger.(ABSTRACT TRUNCATED AT 250 WORDS)