NEUROPEPTIDE-Y (NPY)- AND VASOACTIVE-INTESTINAL-PEPTIDE (VIP)-INDUCEDALDOSTERONE SECRETION BY RAT CAPSULE GLOMERULAR ZONE COULD BE MEDIATED BY CATECHOLAMINES VIA BETA(1) ADRENERGIC-RECEPTORS/

The effects of two Neuropeptide Y(NPY) analogs (Y-1- and Y-2-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 incubat ed in a medium (Krebs-Ringer bicarbonate buffer supplemented with gluc ose and bovine serum albumin) containing or not one of the following s ynthetic peptides: human Leu(31),Pro(34)-NPY (an agonist of the Y-1-ty pe receptors), human/porcine NPY18-36 (an agonist of the Y-2-type rece ptors) and VIP at the concentration of 10(-7) M, associated or not wit h 10(-7) M atenolol (a beta(1) adrenergic antagonist) or ICI-118,551 h ydrochloride (a beta(2) adrenergic antagonist). The two NPY analogs as well as the VIP stimulated the release of catecholamines and of aldos terone. The beta(1) adrenergic antagonist, but not the beta(2) one, wh ich failed to affect basal aldosterone production when given alone, pr evented NPY18-36-, Leu(31),Pro(34)-NPY- or VIP-induced aldosterone sec retion. Present data support the hypothesis that adrenaline and/or nor adrenaline could mediate the effects of both NPY and VIP on aldosteron e secretion via beta(1) adrenergic receptors; alternatively, the stero idogenic effect of NPY or VIP could be related to direct interaction b etween NPY- or VIP-specific binding sites, present on the capsule/glom erular zone of the rat adrenal cortex, and beta(1) adrenergic receptor s. Then the NPYergic, VIPergic and catecholaminergic innervation of th e adrenal cortex, previously characterized by immunohistochemistry, ma y be a potent stimulatory element in the nervous control of the aldost erone secretion.