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Effects of Glucocorticoids on Adrenal Chromaffin Cells
Author(s) -
Hodel A.
Publication year - 2001
Publication title -
journal of neuroendocrinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.062
H-Index - 116
eISSN - 1365-2826
pISSN - 0953-8194
DOI - 10.1111/j.1365-2826.2001.00628.x
Subject(s) - adrenal medulla , endocrinology , medicine , glucocorticoid , catecholamine , chromaffin cell , biology , phenylethanolamine , adrenal cortex , adrenal gland , phenylethanolamine n methyltransferase , glucocorticoid receptor , secretion , downregulation and upregulation , receptor , gene , dopamine , tyrosine hydroxylase , biochemistry
The mammalian adrenal gland consists of two anatomically distinct parts: an outer cortex that synthesizes steroids and a central medulla that contains catecholamine‐producing chromaffin cells. Although derived from different embryological origins, the two secretory tissues in the adult animal are functionally as well as structurally linked. Glucocorticoids, a class of steroid hormones produced by the cortex, exert a variety of effects on medullary chromaffin cells. They modulate the expression of specific genes via activation of glucocorticoid receptors that act as transcription factors and either up‐ or down‐regulate mRNA synthesis. The direct binding to and modulation of cation channels by glucocorticoids as well as the control of mRNA or protein stability are other proposed mechanisms of glucocorticoid action. The activity of phenylethanolamine N ‐methyltransferase, the enzyme that converts noradrenaline into adrenaline, is stimulated by glucocorticoids, which causes the conversion of noradrenergic to adrenergic chromaffin cells. Other phenotypic manifestations of glucocorticoid action include the upregulation of catecholamine synthesis, storage, and secretion. Furthermore, glucocorticoids have been implicated in chromaffin cell differentiation. However, recent gene knockout experiments suggest that glucocorticoid signalling is required only for the acquisition of the adrenergic but not the noradrenergic phenotype.