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The effects of glucocorticoid hormones are thought to be initiated by binding to stereospecific intracellular receptor proteins in target tissues. The kidney enjoys a variety of functions influenced by glucocorticoid hormones. High affinity glucocorticoid receptors have been demonstrated in adrenalectomized rat kidney by the specific binding of dexamethasone (DM). These receptors have been designated Type II, and can be distinguished from high affinity mineralocorticoid receptors (Type I) and the CBGlike corticosterone receptors (Type III) on the basis of differing affinities for a series of physiological and synthetic steroids. By Scatchard plot analysis, the equilibrium (dissociation) constant of the 3HDM–cytoplasmic receptor complex was 5 X 10-9M (25 C), and the concentration of binding sites 1.6 X 10-13 moles per mg protein in the cytoplasmic high speed supernatant (HSS). Similar concentrations of receptor were found in outer cortex and medulla—papilla. The affinity of the Type—II receptor for steroids is in the order DM > corticosterone > desoxycorticosterone ≥aldosterone ≥ cortisol > progesterone > > > estradiol = dihydrotestosterone. Time course studies show a progressive transfer of 3HDM—receptor from cytoplasm to nuclei at 25 C, but not at 0 C. At 25 C the extent of nuclear uptake of 3HDM was a linear function of cytoplasmic 3HDM—receptor concentration over a range of receptor saturation from ∼10 to∼85%. No effect of glucocorticoids upon the kidney has currently been proven to be a direct effect, rather than secondary to glucocorticoid—induced changes elsewhere in the body. The finding of specific renal glucocorticoid receptors, including the nuclear uptake component of the receptor system, supports the possibility of a direct glucocorticoid action in the kidney. (Endocrinology92: 1005, 1973)
Funder et al. (Sun,) studied this question.