The influence of chronic anaemia on catecholamine secretion in the rainbow trout (Oncorhynchus mykiss)

The effect of long-term (7 day) anaemia on catecholamine release was examined in rainbow trout (Oncorhynchus mykiss) in vivo during acute exposure to hypoxia and in situ using a perfused post-cardinal vein preparation. The first goal was to distinguish among reductions in blood O2 partial pressure, O2 concentration and haemoglobin percentage saturation as potential stimuli for, or correlates of, catecholamine secretion during hypoxia. The second goal was to elucidate the role of these factors in promoting enhanced chromaffin cell responsiveness in trout subjected to chronic hypoxia (Montpetit and Perry 1998). Anaemic fish (haematocrit lowered from 28.4±2.4% to 11.9±1.6%) displayed a marked reduction in haemoglobin-O2 binding affinity [P50 (PaO2 at 50% Hb-O2 saturation) was increased from 14.7 mm Hg to 24.3 mm Hg]. Upon exposure to hypoxia, the anaemic fish released catecholamines into their circulation at higher values of arterial O2 partial pressure (∼52 mm Hg versus ∼18 mm Hg) and haemoglobin O2 saturation (<70% versus <55%) than did control fish. In addition, anaemic fish achieved significantly greater circulating levels of total catecholamines (noradrenaline plus adrenaline) during acute hypoxia (294.8±67.3 versus 107.0±35.6 nmol l−1). These results do not support the view that catecholamine release is triggered by a reduction in haemoglobin O2 saturation or arterial PO2, per se. Nor are they consistent with the idea that catecholamine release occurs at a threshold value of arterial PO2 corresponding to a critical reduction in blood O2 concentration. The effects of the non-selective cholinergic receptor carbachol on catecholamine secretion from chromaffin tissue were assessed using perfused posterior cardinal vein preparations derived from control or anaemic fish. For adrenaline secretion, there was no statistically significant change in the ED50 (dose eliciting 50% response). For noradrenaline secretion however, preparations originating from anaemic fish displayed an enhanced responsiveness to carbachol as indicated by a significant 4.5-fold reduction in the carbachol ED50 value from 2.53 × 10−6 mol kg−1 to 5.67 × 10−7 mol kg−1. These results demonstrate that anaemia-induced hypoxaemia, in the absence of any lowering of PO2, is able to modulate the responsiveness of chromaffin cells to cholinergic stimulation.