Abstract

AbstractThe 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.

Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.