Ontogeny of adrenomedullary responses to hypoxia and hypoglycemia: role of splanchnic innervation.
Adrenals of neonatal rats were denervated at 3 days of age (just before functional neuronal connections are ordinarily made). At 14 days of age, rats with denervated adrenals did not secrete catecholamines in response to a neurogenic reflex stimulus (insulin-induced hypoglycemia), confirming that innervation had failed to develop; sham-operated littermates were fully responsive to insulin. In contrast, hypoxia was still able to cause depletion of adrenal catecholamines in the denervated group, indicating the persistence of a non-neurogenic secretory mechanism well past the age at which it should have disappeared (8 days). Prolonged deprivation of neural input in adult rats also led to the re-emergence of non-neurogenic capabilities. Twenty-one days after surgery in adulthood, adrenal responses to insulin were still not present but those to hypoxia were. Thus, the development of neural stimulation itself is responsible for the ontogenetic loss of the immature type of adrenal catecholamine release mechanism and does so by suppressing the non-neurogenic component; consequently the mechanism can reappear when nerve traffic is interrupted for extended periods.
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