This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Copyright Permission Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by FUNDER, J. W. Articles by EDELMAN, I. S. Search for Related Content PubMed PubMed Citation Articles by FUNDER, J. W. Articles by EDELMAN, I. S.

Glucocorticoid Receptors in Rat Kidney: The Rinding of Tritiated-Dexamethasone¹

Cardiovascular Research Institute and the Departments of Medicine, and of Biochemistry and Biophysics, University of California School of Medicine San Francisco

Abstract

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 to85%. 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. (Endocrinology 92: 1005, 1973)

Footnotes

¹ With the financial support of USPHS, National Heart and Lung Institute, Grant No. HL–06285.

² During the tenure of a National Heart Foundation of Australia Overseas Research Fellowship.

³ During the tenure of a post-doctoral traineeship provided by USPHS National Heart and Lung Institute, Grant No. HL–05725.

Received July 3, 1972.

This article has been cited by other articles:

				J. Funder, P. Pearce, R Smith, and A. Smith Mineralocorticoid action: target tissue specificity is enzyme, not receptor, mediated Science, October 28, 1988; 242(4878): 583 - 585. [Abstract] [PDF]

				J. Funder Adrenal steroids: new answers, new questions Science, July 17, 1987; 237(4812): 236 - 237. [PDF]