||Northrop Services, Inc./Environmental Sciences, Research Triangle Park, NC. ;Medical Coll. of Pennsylvania, Philadelphia. ;Duke Univ. Medical Center, Durham, NC.;Health Effects Research Lab., Research Triangle Park, NC.
In the mature rat, reflex sympathetic stimulation by insulin-induced hypoglycemia resulted in profound depletion of adrenal epinephrine, and to a lesser extent, Norepinephrine. In the developing rat, insulin evoked little or no secretory response from the adrenals prior to 1 week of age. By 7 days, a moderate depletion of epinephrine was seen and the magnitude of the response increased with age. In contrast, during the first 3 weeks of postnatal life, insulin failed to deplete norepinephrine from the adrenal medulla and in fact, produced an increase. The results suggest that the ontogeny of the two chromaffin cell types (norepinephrine and epinephrine-containing) in the adrenals and the maturation of their secretory responses are under differential regulation. Because descending supraspinal catecholaminergic and serotonergic systems have been implicated to play key roles in regulating adrenomedullary function, the ontogeny of the sympatho-adrenomedullary axis was evaluated after neonatal central lesioning with 6-hydroxydopamine or 5,7-dihydroxytryptamine. The results suggest that central monoaminergic neurons impose both inhibitory and facilitatory influences on the maturation of specific chromaffin cell types in the adrenal medulla and that supraspinal catecholaminergic inputs may play a role in determining the set-point for reflex adrenomedullary responses. (Copyright (c) 1987 IBRO.)