“…In rabbits prolonged administration of aldosterone produced ; marked falls in plasma potassium and magnesium concentrations (Rettori et al 1969) and significant increase in RBC sodium content, probably due to an increase in RBC membrane permeability to sodium. In previous experiments, we demonstrated that long-term administration of aldosterone in rabbits produced a significant increase of RBC sodium content (Afifi et al 1979). We suggest that, the increase in RBC sodium content in the presence of untreated liver cirrhosis and ascites may be due to a secondary hyperaldosteronism in these patients.…”