Endothelins as local activators of adrenocortical cells

Journal of Molecular Endocrinology - Tập 32 Số 1 - Trang 1-7 - 2004
Catherine Delarue1, J. Michael Conlon2, Isabelle Rémy‐Jouet3,4,5, Alain Fournier6, Hubert Vaudry7
1European Institute for Peptide Research (IFRMP 23), Laboratory of Cellular and Molecular Neuroendocrinology, INSERM U-413, UA CNRS, University of Rouen, 76821, Mont-Saint-Aignan, France
2Department of Biochemistry, Faculty of Medicine and Health Sciences, United Arab Emirates University, PO Box 17666, Al-Ain, United Arab Emirates
3European Institute for Peptide Research (IFRMP 23), Laboratory of Cellular and Molecular Neuroendocrinology, INSERM U-413, UA CNRS,
4INRS-Institut Armand Frappier
5University of Rouen, 76821 Mont-Saint-Aignan, France
6INRS/Institut Armand Frappier, University of Québec, Pointe-Claire, Québec, Canada H9R
7University of Rouen#TAB#

Tóm tắt

Besides the classical corticotropic hormones, ACTH and angiotensin II, various regulatory peptides produced by the adrenal gland are thought to participate in the control of corticosteroid secretion. Here, we review the evidence that endothelins (ETs) synthesized within the adrenal cortex may act as autocrine and/or paracrine factors to regulate adrenocortical cell activity. The expression of ETs has been detected in normal, hyperplastic and neoplastic adrenocortical cells. The occurrence of ET receptors has been described in the different zones of the cortex. ETs stimulate the secretion of both glucocorticoids and mineralocorticoids, and modulate the proliferation of adrenocortical cells. The effects of ETs on steroidogenic cells are mediated through the activation of various signaling mechanisms including stimulation of phospholipase C, phospholipase A2 and adenylyl cyclase activity, as well as calcium influx through plasma channels. These observations suggest that locally produced ETs may play an important role in the regulation of corticosteroid secretion and in the control of mitogenesis in normal and tumoral adrenocortical cells.

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