Beta-adrenergic control of blood oxygen affinity in acutely hypoxia exposed rainbow trout.

Acute exposure of rainbow trout to hypoxic water (PwO2 = 40 mmHg, 15 degrees C) caused a significant (P less than 0.01) increase in blood O2 affinity, from the normoxic P50 value (at pHc 7.93) of 23.2 +/- 1.1 mmHg to about 19 mmHg, within 5 min. Specimens injected with the beta-antagonist propranolol showed no change in blood P50, despite a more pronounced reduction of arterial PO2 during the hypoxic exposure. The change in blood P50 coincided with an increase in plasma catecholamines, notably noradrenaline. There was no change in the molar ratios of ATP:Hb4 and GTP:Hb4. The altered blood P50, however, correlated with an alkalinization and an increased sodium concentration of the red cells. This red cell alkalinization can be explained by beta-adrenergic stimulation of a membrane bound Na+/H+ antiporter. Propranolol injection into normoxic resting trout caused a significant decrease in PaO2 and increase in PaCO2 indicating beta-adrenergic control of gas exchange in the gills.