Abstract

The direct influence of aldosterone on the human and avian red blood cell (RBC) transport systems, Na<sup>+</sup>/K<sup>+</sup> pump, Na<sup>+</sup>,K<sup>+</sup>,2Cl<sup>-</sup> symporter, and K<sup>+</sup> (Na<sup>+</sup>)/H<sup>+</sup> exchanger, was investigated with tracer kinetics. The present work proved that aldosterone has no significant effect on these transport pathways. However, in young human RBCs containing reticulocytes aldosterone showed a significant inhibition of the Na<sup>+</sup>,K<sup>+</sup>,2Cl<sup>-</sup> symporter. Investigations of the Li<sup>+</sup> efflux via the Na<sup>+</sup>/Li<sup>+</sup> exchanger using atom absorption spectroscopy revealed that aldosterone has no effect on this transporter. Studies of the effect of aldosterone on the Ca<sup>2+</sup> content and the intracellular pH (pH<sub>i</sub>) were carried out on single RBCs with a fluorescence imaging system. Both parameters are affected by aldosterone. The Ca<sup>2+</sup> uptake in the presence of aldosterone, under conditions where the Ca<sup>2+</sup> pump is inhibited, showed marked differences from the control. Since the effect is nifedipine-sensitive, it seems that aldosterone affects a Ca<sup>2+</sup> channel. In addition, aldosterone leads to an acidification of the intracellular medium after an initial alkalisation due to an effect on the Na<sup>+</sup>/H<sup>+</sup> exchanger.

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