ISSN 1470-3947 (print) | ISSN 1479-6848 (online)

Endocrine Abstracts (2019) 63 PL5 | DOI: 10.1530/endoabs.63.PL5

Paracrine regulation of the adrenal cortex

Dr Hervé Lefebvre


Numerous <i>in vitro</i>studies have shown that the secretory activity of the human adrenal cortex is activated by a wide variety of neuropeptides and conventional neurotransmitters released in the vicinity of adrenocortical cells by chromaffin cells, endothelial cells, adipocytes, cells of the immune system and nerve endings. The role of these paracrine factors in the physiological control of the adrenocortical function remains unclear, especially for cortisol production which is principally dependent on ACTH secretion. However, it appears likely that intraadrenal bioactive signals are involved in the regulation of aldosterone secretion which is partly independent of the renin-angiotensin system. In particular, increasing evidence indicates that aldosterone production is stimulated by neural inputs, leptin and serotonin (5-HT) released by subcapsular mast cells. Interestingly, the occurrence of paracrine regulatory processes has also been reported in adrenocortical hyperplasias and tumors responsible for aldosterone or cortisol excess. These mechanisms roughly involve the same actors as those operating in the normal adrenal but exhibit alterations at various levels which tend to reinforce their potency to increase steroid production. The main defects in the intraadrenal control systems noticed so far include hyperplasia of cells producing the paracrine factors and illicit expression of the latter and their receptors. This new pathophysiological concept is nicely illustrated by mast cell hyperplasia in aldosterone-producing adenomas (APAs) and upregulation of the 5-HT signaling pathway or ectopic synthesis of ACTH in adrenocortical cells in bilateral adrenal hyperplasias responsible for cortisol excess. Upregulated paracrine factors and their receptors are likely to play a significant role in adrenocortical hyperplasia/tumor expansion and associated steroid hypersecretion together with somatic mutations affecting the calcium signaling pathway in APAs or the cAMP/protein kinase A pathway in cortisol-producing adenomas. They also represent new targets for the pharmacological treatment of primary adrenal steroid excess.

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