In neonatal animals, when in some species (rat and human) the splachnic innervation is not functional, hypoxia and hypercapnia/acidosis elicit directly the secretion of catecholamine (CA) from the chromaffin cells (non neurogenic). The resulting high plasmatic CA concentration produce metabolic, cardio- circulatory and ventilatory effects that are important for adapting to the extrauterine life. We have explored whether hypoglycemia, that is very common in neonates, also promotes the increase of CA secretion acting directly on chromaffin cells at this age and the mechanisms involved. We have used an in vitro preparation designed to record by amperometry the secretory responses from rat adrenal medulla (AM).

We have found that perfusion of AM with solution containing low glucose (2.5, 1.0 and 0 mM glucose, 5min) elicit in a neonatal AM (1-2 days) a transitory increase of CA secretion similar to hypoxic stimulation that was dose-dependent. This secretion was almost abolished in the absence of extracellular calcium and in the presence of nisoldipine (5mM) and was not prevented by the addition of 5-10 mM piruvate. Responses were also present in juvenile AM (14-15 days) after splachnic innervation was functional. Finally, we observed that association of hypoxic and hypoglycemic stimuli potenciates the secretory response in neonatal AM. The synergistic effect between hypoglycemia and hypoxia, that reproduces episodes that occurs in the fetus during natural delivery, would explain the CA outburst seen in just-born mammals, which seems to be crucial for adaptation to extrauterine life. Supported by Spanish MEC (SAF 2006-00146).