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Atrial natriuretic peptide enhances cortisol secretion from guinea-pig adrenal gland: Evidence for an indirect paracrine mechanism probably involving the local release of medullary catecholamines

Atrial natriuretic peptide (ANP) is a regulatory hormone widely expressed, along with its receptors, in organs and body tissues. ANP is well known to inhibit aldosterone secretion from mammalian adrenals, but its effect on glucocorticoid-hormone production is controversial. In vivo experiments showe...

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Published in:International journal of molecular medicine 2006-04, Vol.17 (4), p.633-636
Main Authors: Raha, Dipali, Tortorella, Cinzia, Neri, Giuliano, Prasad, Anita, Raza, Bushra, Raskar, Ranu, Dubey, Rakhi, Sen, Nisarga, Macchi, Carlo, Malendowicz, Ludwick, Ahmad, M, Nussdorfer, Gastone
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Language:English
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Summary:Atrial natriuretic peptide (ANP) is a regulatory hormone widely expressed, along with its receptors, in organs and body tissues. ANP is well known to inhibit aldosterone secretion from mammalian adrenals, but its effect on glucocorticoid-hormone production is controversial. In vivo experiments showed that prolonged ANP administration raised the plasma concentration of cortisol in both normal and dexamethasone/captopril-treated guinea pigs (i.e. in animals with pharmacologically interrupted hypothalamic-pituitary-adrenal axis and renin-angiotensin system). ANP did not affect cortisol secretion from dispersed guinea pig zona fasciculata-reticularis cells, but enhanced catecholamine release from adrenomedullary cells. ANP stimulated cortisol output from guinea pig adrenal slices containing medullary chromaffin tissue, and the β-adrenoceptor antagonist l-alprenolol blocked this effect. The conclusion is drawn that ANP, when the structural integrity of the adrenal gland is preserved, is able to enhance glucocorticoid secretion in guinea pigs, through an indirect mechanism involving the rise in the catecholamine release, which in turn, acting in a paracrine manner, stimulate secretion of inner adrenocortical cells.
ISSN:1107-3756
1791-244X
DOI:10.3892/ijmm.17.4.633