Abstract

Red blood cells from rainbow trout rely mainly on oxidative phosphorylation to cover the energy demand of processes such as cation transport and protein synthesis. Stimulation of these cells with catecholamines leads to an increase in the intracellular Na + concentration due to adrenergic activation of the erythrocyte Na +–H + exchanger. Adrenergic stimulation also increases red cell oxidative phosphorylation which largely can be ascribed to increased activity of the Na +–K + pump in response to the increase in intracellular Na + concentration. Based on experiments with the Na +-ionophore, monensin, it has been suggested that adrenergic stimulation is a prerequisite for the increase in oxidative ATP-production observed when intracellular Na + is increased. Using washed red blood cells from rainbow trout, the present study examines the role for adrenergic stimulation in the metabolic response when intracellular Na + is elevated. It is shown that while monensin (5×10 −8–5×10 −6 M) causes a persistent up-to-12-fold increase in the intracellular Na + concentration, it only transiently elevates the activity of the Na +–K + pump. Furthermore, monensin (5×10 −6 M) decreased rather than increased red cell oxygen uptake. In contrast, adrenergic stimulation, which produced a 4-fold elevation in intracellular Na +, led to a 2.5-fold increase in red cell oxygen uptake and an 11-fold increase in Na +–K + pump activity. Forty percent of the increase in oxygen uptake was blocked by inhibition of the Na +–K + pump. In monensin-treated cells, adrenergic stimulation was, however, without effect on oxygen uptake and Na +–K + pump activity. These data do not support the theory that adrenergic stimulation has a direct effect on the ATP-producing processes of trout red blood cells but rather suggest that the effect of catecholamines on oxygen uptake is restricted to effects on the energy-consuming processes of the cells.

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