Tissue differences in the up-regulation of glucocorticoid-binding proteins in the rat.

The magnitude of increase in glucocorticoid receptor concentration and transcortin-like binding was examined in a variety of peripheral tissues and brain structures after adrenalectomy. Glucocorticoid binding was assayed in liver, heart, kidney, pituitary, hippocampus, cerebral cortex, amygdala-entorhinal area, and hypothalamus. Glucocorticoid receptor concentration, measured using [3H]dexamethasone as ligand, increased in all eight tissues, but the magnitude of this increase varied 30-fold among tissues. The largest increase was shown by kidney cytosol, followed by amygdala-entorhinal cortex, hippocampus, liver, cerebral cortex, hypothalamus, pituitary, and heart. These increases were not due to a selective enhancement of mineralocorticoid receptors. The increase in transcortin in peripheral tissues was variable and exceeded the increase in plasma transcortin by an order of magnitude. It was concluded that up-regulation of the glucocorticoid receptor after adrenalectomy is a response common to most, if not all, glucocorticoid target tissues. However, the magnitude of this response was tissue specific and was not directly related to initial receptor density. The marked increase in tissue transcortin ([3H]corticosterone binding in the presence of excess dexamethasone) suggested that plasma transcortin is sequestered by peripheral tissues in substantial amounts in the acutely adrenalectomized rat. The increase in transcortin uptake by tissues and the increases in cytosolic receptor number are apparently subject to different regulatory control.