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Summary: It is well known that adrenergic stimulation of fish red blood
cells (RBCs) increases the internal pH and thus enhances the
affinity of haemoglobin for oxygen under extreme conditions
of hypoxia (Cossins and Richardson, 1985; Thomas and Perry,
1992). The results of in vitro and in vivo studies have
established that the mechanism promoting intracellular
alkalization is a catecholamine-mediated activation of the
Na+/H+ exchanger via stimulation of the -adrenoreceptors
(Motais and Garcia-Romeu, 1987; Nikinmaa and Tufts, 1989;
Nikinmaa, 1992; Guizouarn et al. 1993). The increase in
intracellular Na+ concentration that follows adrenergic
stimulation induces a water inflow which causes cell swelling.
The RBCs may then recover their resting Na+ concentration,
cell volume and electrochemical potentials by means of passive
(Borgese et al. 1987a; Thomas and Perry, 1992; Guizouarn et
al. 1993) and active (Tufts and Boutilier, 1991) transport,
which increases ATP consumption (Salama and Nikinmaa,
1988; Ferguson and Boutilier, 1988, 1989; Ferguson et al.
1989; Tufts and Boutilier, 1991). The energy equilibrium of
the cell can be maintained provided that the rate of ATP
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