Cushing's syndrome variants secondary to aberrant hormone receptors.

Abstract

The secretion of cortisol and other steroids from adrenal tumors can be regulated by hormones other than corticotropin following the aberrant expression of several G-protein-coupled receptors (GPCRs). To date, ectopic receptors for gastric inhibitory polypeptide, beta-adrenergic receptor agonists, vasopressin (V(2) and V(3) receptors), 5-hydroxytryptamine (5-HT(7) receptor) and, probably, angiotensin II (AT(1) receptor) have been identified. Either increased expression or altered activity of eutopic receptors for vasopressin (V(1)), luteinizing hormone/human chorionic gonadotropin, 5-HT (5-HT(4) receptor) and leptin might also be involved. One or more aberrant receptors can be present in unilateral tumors and bilateral macronodular adrenal hyperplasia, at either the early subclinical or overt stages of hormone secretion. The identification of aberrant adrenal GPCRs offers the potential for novel pharmacological therapies that either suppress the endogenous ligands or block the receptor with specific antagonists.

• Authors: André Lacroix, Valérie Baldacchino, Isabelle Bourdeau, Pavel Hamet, Johanne Tremblay
• Journal: Trends in endocrinology and metabolism: TEM (Trends Endocrinol Metab) Vol. 15 Issue 8 Pg. 375-82 (Oct 2004) ISSN: 1043-2760 [Print] United States
• PMID: 15380809 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Review)

Chemical References

• Receptors, Cell Surface
• Receptors, G-Protein-Coupled

Topics

• Cushing Syndrome (drug therapy, physiopathology)
• Humans
• Receptors, Cell Surface (metabolism)
• Receptors, G-Protein-Coupled (metabolism)