It has been suggested that in or on erythrocytes there is a substance capable of binding cortisol as strongly as transcortin but having a lower capacity than the latter (Sandberg, Slaunwhite & Carter, 1960; De Moor, Heirwegh, Heremans & Declerck-Raskin, 1962; De Moor & Steeno, 1962). Such a binding agent should compete with plasma transcortin and thus influence cortisol distribution between erythrocytes and plasma. Since the capacity of the hypothetical agent is said to be low (Sandberg et al. 1960), competition must be looked for at low cortisol levels. The authors have used corticoid-poor (12 p.m.) blood to study this aspect of corticoid distribution. With fluorimetric techniques a definite upswing of the erythrocyte uptake curve was noted at a mean plasma corticoid level of 7·1 μg./100 ml. (De Moor & Steeno, 1962). Since this could be due to differences in the specificity of both fluorimetric techniques, experiments with tritium-labelled steroids
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