The purpose of this study was to evaluate the relationship between neuroendocrine function and the beta receptor activity of the lung in a group of 47 pediatric patients with bronchial asthma. It is postulated that since hypothalamic norepinephrine (NE) is known to inhibit corticotropin-releasing hormone (CRH), an increase in brain NE as measured by its metabolite 3-methoxy-4-hydroxy-phenylglycol (MHPG) could reflect the depression of the hypothalamic-pituitary-adrenal (HPA) axis as measured by urinary cortisol levels. Further, since cortisol influences epinephrine formation in the adrenal medulla and since cortisol and epinephrine contribute to beta receptor function, it is further postulated that an increase in brain NE by depressing the HPA axis could thereby, cause a relative decrease in both cortisol and epinephrine with resultant beta receptor dysfunction. In both age groups, the 3- to 11-year-olds and the adolescents, differences in NE were found among the three subgroups (P = .003) with the difference observed only between the wheezing (decreased NE) and control groups (P less than .05). There was a similar difference in MHPG (elevated) among these groups. In a similar manner, the MHPG/NE ratios (elevated) were statistically different in comparing the three groups in the 3- to 11-year-old range. In the adolescent group both the wheezing and nonwheezing groups were comparably elevated and showed statistically significant differences from their controls. The results of this study appear to support the hypothesis and suggests that brain NE may play a pivotal role in the beta-adrenergic dysfunction characteristic of bronchial asthma.