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

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Summary

Acute exposure of rainbow trout to hypoxic water (\(Pw_{{\text{O}}_2 }\)=40 mmHg, 15 °C) caused a significant (P<0.01) increase in blood O2 affinity, from the normoxicP 50 value (at pHe 7.93) of 23.2±1.1 mmHg to about 19 mmHg, within 5 min. Specimens injected with the β-antagonist propranolol showed no change in bloodP 50, despite a more pronounced reduction of arterial\(P_{{\text{O}}_2 }\) during the hypoxic exposure.

The change in bloodP 50 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 bloodP 50, however, correlated with an alkalinization and an increased sodium concentration of the red cells. This red cell alkalinization can be explained by β-adrenergic stimulation of a membrane bound Na+/H+ antiporter.

Propranolol injection into normoxic resting trout caused a significant decrease in\(Pa_{{\text{O}}_2 }\) and increase in\(Pa_{{\text{CO}}_2 }\) indicating β-adrenergic control of gas exchange in the gills.

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Tetens, V., Christensen, N.J. Beta-adrenergic control of blood oxygen affinity in acutely hypoxia exposed rainbow trout. J Comp Physiol B 157, 667–675 (1987). https://doi.org/10.1007/BF00700988

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