Catecholamine release controlled by blood oxygen tension during deep hypoxia in trout: effect on red blood cell Na/H...

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 (PaO2) reached around 15 Torr (Thomas S., Respir. Physiol. 74, 77-90, 1988). This blood pH drop coincided with a marked increase in plasma catecholamine levels. The catecholamine secretion was transient and the hormones were cleared provided PaO2 remained above 10 Torr. On the other hand, when PaO2 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 PaO2 remains above or below 10 Torr respectively, as previously described. Following the transient hormone peak when PaO2 stabilized above 10 Torr, it was possible to trigger the second pattern of continuous catecholamine secretion by controlling water PO2 so that PaO2 declined below 10 Torr. We conclude that the blood oxygen level controls catecholamine secretion during deep hypoxia.