Neuropeptide Y (NPY)- and vasoactive intestinal peptide (VIP)-induced aldosterone secretion by rat capsule/glomerular zone could be mediated by catecholamines via beta 1 adrenergic receptors.
The effects of two Neuropeptide Y (NPY) analogs (Y1- and Y2-type) and vasoactive intestinal peptide (VIP) on both catecholamine (adrenaline and noradrenaline) release and aldosterone production by rat adrenal capsule/glomerular zone, have been investigated in vitro. The adrenal capsule/glomerular zones, collected from adult male rats, were incubated in a medium (Krebs-Ringer bicarbonate buffer supplemented with glucose and bovine serum albumin) containing or not one of the following synthetic peptides: human Leu31,Pro34-NPY (an agonist of the Y1-type receptors), human/porcine NPY18-36 (an agonist of the Y2-type receptors) and VIP at the concentration of 10(-7) M, associated or not with 10(-7) M atenolol (a beta 1 adrenergic antagonist) or ICI-118,551 hydrochloride (a beta 2 adrenergic antagonist). The two NPY analogs as well as the VIP stimulated the release of catecholamines and of aldosterone. The beta 1 adrenergic antagonist, but not the beta 2 one, which failed to affect basal aldosterone production when given alone, prevented NPY18-36-, Leu31,Pro34-NPY- or VlP-induced aldosterone secretion. Present data support the hypothesis that adrenaline and/or noradrenaline could mediate the effects of both NPY and VIP on aldosterone secretion via beta 1 adrenergic receptors; alternatively, the steroidogenic effect of NPY or VIP could be related to direct interaction between NPY- or VIP-specific binding sites, present on the capsule/glomerular zone of the rat adrenal cortex, and beta 1 adrenergic receptors. Then the NPYergic, VIPergic and catecholaminergic innervation of the adrenal cortex, previously characterized by immunohistochemistry, may be a potent stimulatory element in the nervous control of the aldosterone secretion.
Bernet
F
F
Neuroendocrinologie du Développement, Université de Lille, Villeneuve d'Ascq, France.
Bernard
J
J
Laborie
C
C
Montel
V
V
Maubert
E
E
Dupouy
J P
JP
D000311:Adrenal Glands / Q000187:drug effects / Q000378:metabolism*; D058671:Adrenergic beta-1 Receptor Antagonists; D000450:Aldosterone / Q000378:metabolism*; D000818:Animals; D001262:Atenolol / Q000494:pharmacology; D001345:Autoradiography; D002395:Catecholamines / Q000502:physiology*; D004837:Epinephrine / Q000378:metabolism / Q000502:physiology; D066298:In Vitro Techniques; D008297:Male; D009478:Neuropeptide Y / Q000031:analogs & derivatives / Q000494:pharmacology*; D009638:Norepinephrine / Q000378:metabolism / Q000502:physiology; D011412:Propanolamines / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D018342:Receptors, Adrenergic, beta-1 / Q000187:drug effects / Q000502:physiology*; D014660:Vasoactive Intestinal Peptide / Q000031:analogs & derivatives / Q000494:pharmacology*; D015384:Zona Glomerulosa / Q000187:drug effects / Q000378:metabolism*
D058671:Adrenergic beta-1 Receptor Antagonists; D002395:Catecholamines; D009478:Neuropeptide Y; D011412:Propanolamines; D018342:Receptors, Adrenergic, beta-1; D014660:Vasoactive Intestinal Peptide; C026777:ICI 118551; D000450:Aldosterone; D001262:Atenolol; D009638:Norepinephrine; D004837:Epinephrine