Developmental regulation of glucosensing in rat adrenomedullary chromaffin cells

Abstract

During birth, asphyxial stimuli such as hypoxia and acid hypercapnia trigger the release of catecholamines (CAT) from adrenomedullary chromaffin cells (AMCs), which protects the heart and prepares the lungs of the neonate for air breathing. These direct chemosensing properties are present in neonatal AMCs but are lost by ~2 weeks postnatally, as these cells become innervated by the splanchnic nerve. Asphyxia also leads to glucose deprivation though it is unknown whether or not neonatal AMCs are also directly sensitive to low glucose (hypoglycemia). Recently, we demonstrated that 0 glucose induced membrane depolarization and a rise in intracellular Ca2+ in an immortalized, fetal‐derived chromaffin cell line. In the present study, we tested the hypothesis that primary neonatal rat AMCs are sensitive to hypoglycemia and that this property is developmentally regulated. Using fura‐2 Ca2+ imaging and carbon fiber amperometry we found that hypoglycemia induced a rise in intracellular Ca2+ and quantal vesicular CAT secretion in most neonatal AMCs. Furthermore, these responses were markedly reduced or absent in 2‐week old juvenile AMCs. Though the molecular mechanisms remain to be elucidated, this study suggests that the neonatal rat adrenal medulla may act as a glucosensor, perhaps similar to that recently proposed for the carotid body. This work was supported by the Heart and Stroke Foundation of Ontario and NSERC.