The influence of transcortin-binding capacity on corticosterone tissue uptake and degradation in the infant rat were studied. It was shown that the T4-induced increase of plasma transcortin level did not alter the corticosterone half-life, but caused a reduction of the virtual volume of distribution and, as a consequence, of the hormone metabolic clearance rate. From a comparison between in vivo and in vitro tissue uptake of the steroid, it was concluded that plasma transcortin binding sites strongly compete with tissue binding sites. In addition, some of the findings would suggest that the liver may not store transcortin, as a molecule exhibiting the same characteristics as the plasma counterpart.