Plasma catecholamines in patients with Addison's disease.

Abstract

Two endocrine tissues are present within the adrenal gland: the steroid producing cortical cells and the catecholamine producing chromaffin cells. Glucocorticoids occur in high concentrations in the adrenal medulla. In vitro, glucocorticoids have been shown to induce the enzyme phenyl-N-methyl-transferase which is necessary for the production of adrenaline in adrenal medullary cells. The purpose of this study was to evaluate the possible significance of a local glucocorticoid effect on adrenomedullary function. Plasma catecholamine levels were measured in patients with autoimmune Addison's disease where local production of corticosteroids is deficient in the presence of intact chromaffin tissue. Catecholamines were measured by high pressure liquid chromatography and ACTH, renin and adrenal steroids by radioimmunoassay. Nineteen Addisonian patients (9 females, 10 males) were treated according to a standard regime with oral cortisone acetate (37.5 mg/day) and fludrocortisone (0.1 mg/day). All patients were clinically well. Mean plasma adrenaline in patients with Addison's disease was significantly reduced compared to a sex and age matched control group (males (n = 10) 143 +/- 36 pmol/l, controls (n = 27) 303 +/- 30 pmol/l, P < 0.01; females (n = 9) 77 +/- 25 pmol/l, controls (n = 27) 293 +/- 21 pmol, P < 0.001). The noradrenaline:adrenaline ratio was clearly higher in patients with Addison's disease (males 24 +/- 4, controls 9 +/- 1, P < 0.01; females 45 +/- 6, controls 9 +/- 1, P < 0.01). We conclude that the physiologically high local glucocorticoid concentration may be responsible for normal adrenaline production under basal conditions.