Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2004) 8 S8

1Laboratory of Cellular and Molecular Neuroendocrinology, INSERM U 413, IFRMP 23, University of Rouen, 76821 Mont-Saint-Aignan, France; 2Service of Endocrinology, Faculty of Medicine, University of Sherbrooke, Sherbrooke, Quebec, Canada.


There is now clear evidence that diverse corticotropic factors released by chromaffin cells, by nerve fibers innervating the adrenal cortex, by cells of the immune system and/or by the endothelium are involved in the local control of adrenocortical cell activity. The adrenal gland of lower vertebrates, notably amphibians, in which cortical and chromaffin cells are closely entangled, is a very suitable model to investigate the paracrine regulation of adrenocortical cells. The examples of serotonin (5-HT) and pituitary adenylate cyclase-activating polypeptide (PACAP) will be used to illustrate the roles played by neurotransmitters and neuropeptides in the complex neuroendocrine control of adrenocortical cells and to illuminate the intriguing species-specific mechanisms involved in this paracrine mode of regulation. Thus, 5-HT, produced by chromaffin cells in the frog, chromaffin cells and mast cells in the rat, and only by mast cells in the human adrenal gland, stimulates corticosteroid secretion through activation of 5-HT4 receptors in frog and human, and through 5-HT7 receptors in rat. On the other hand, PACAP, released from nerve fibers in the frog, or produced by chromaffin cells in the mammalian adrenal gland, acts either directly on adrenocortical cells in frog or indirectly through the local release of catecholamines in mammals. The occurrence of 5-HT4 receptors in ACTH-independent macronodular hyperplasia and in Conn's adenoma, and the presence of PACAP receptors in the adrenal medulla of the human fetus, strongly suggest that neurotransmitters and neuropeptides may also play a crucial role in the pathogenesis of adrenal diseases as well as in the ontogeny of the adrenal gland.

Supported by grants from INSERM (U413) and the Conseil Regional de Haute-Normandie.

Volume 8

195th Meeting of the Society for Endocrinology joint with Diabetes UK and the Growth Factor Group

Society for Endocrinology 

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