SHORT COMMUNICATION DOWN-REGULATION OF RED BLOOD CELL b-ADRENORECEPTORS IN RESPONSE TO CHRONIC ELEVATION OF PLASMA CATECHOLAMINE LEVELS IN THE RAINBOW TROUT

In many teleost fish, including the rainbow trout, Oncorhynchus mykiss, catecholamines are mobilized into the blood in situations when enhanced oxygen transport is necessary, such as hypoxia, anaemia, hypercapnia and strenuous exercise (see review by Thomas and Perry, 1992). These hormones initiate a series of integrated physiological responses that optimize cardiovascular and respiratory functions (see reviews by Perry and Wood, 1989; Randall and Perry, 1992; Thomas and Perry, 1992). Stimulation of red blood cell b-adrenoreceptors leads to the activation of a red blood cell membrane Na+/H+ antiporter which extrudes protons in exchange for plasma Na+, thereby elevating intracellular pH (pHi) (Baroin et al. 1984; Cossins and Richardson, 1985; see review by Nikinmaa, 1992). The binding of catecholamines to badrenoreceptors, which are coupled to adenylate cyclase, engenders the formation of cyclic AMP. This second messenger, in turn, presumably initiates a phosphorylation cascade which ultimately activates the Na+/H+ antiporter. Erythrocyte alkalization can increase haemoglobin oxygen-binding affinity and capacity via the Bohr and Root effects, thus increasing the ability of the blood to transport oxygen (Tufts and Randall, 1989; see also reviews by Nikinmaa and Tufts, 1989; Perry and Wood, 1989; Randall and Perry, 1992; Thomas and Perry, 1992). Chronic elevation of plasma catecholamine concentrations appears to attenuate the red blood cell adrenergic response. Rainbow trout exposed to moderate levels of hypoxia (water partial pressure of oxygen 6.7–9.3 kPa) for 48 h exhibited elevated plasma adrenaline levels, and the sensitivity of red blood cell Na+/H+ exchange to exogenous adrenaline, in vitro, was reduced by 60–100 % (Thomas et al. 1991). Further, the intensity of proton extrusion in response to adrenaline addition was found to be inversely correlated to the endogenous plasma adrenaline concentration (Thomas et al. 1991). Thomas and co-workers suggested that a reduction in functional red blood cell