CATECHOLAMINE RELEASE CONTROLLED BY BLOOD-OXYGEN TENSION DURING DEEP HYPOXIA IN TROUT - EFFECT ON RED-BLOOD-CELL NA/H EXCHANGER ACTIVITY

Changes in plasma catecholamine levels were measured in trout exposed to acute hypoxia, in order to correlate with acid-base disturbances due to activation of the cAMP-dependent Na+/H+ antiporters of red blood cells, as previously described (Fiévet B., Respir. Physiol. 74, 99-114, 1988). The extracellular acidosis corresponding with the stimulation of the exchangers, occurred when arterial oxygen partial pressure (PaO) reached around 15 Torr (Thomas S., Respir. Physiol. 74, 77-90, 1988). This blood pH drop coincide with a marked increase in plasma catecholamine levels. The catecholamine secretion was transient and the hormones were cleared provided PaO remained above 10 Torr. On the other hand, when PaO remained below 10 Torr, there was a persistent secretion of catecholamines. This is in agreement with the fact that the exchangers are 'turned off' or sustained when PaO remains above or below 10 Torr respectively, as previously described. Following the transient hormone peak when PaO stabilized above 10 Torr, it was possible to trigger the second pattern of continuous catecholamine secretion by controlling water PO so that PaO declined below 10 Torr. We conclude that the blood oxygen level controls catecholamine secretion during deep hypoxia. © 1990.