Phenylethanolamine N-methyltransferase (PNMT, E.C.2.1.1.28) is the terminal enzyme in the synthesis of adrenaline ill the adrenal medulla 1, other chromaffin tissues, and in the mammalian brain iv. Changes in the level of adrenal and hypothalamic PNM T activity have been correlated with changes in the tissue content of adrenaline 13,15,1s,2°. It is well established that PNMT requires glucocorticoids for maximal activity. The synthetic glucocorticoid, dexamethasone, has been shown to induce adrenal PNMT in hypophysectomized rats ~9 and to stimulate the enzyme in extra-adrenal chromaffin tissue of neonatal rats~, 6 and brain of adult rats 13. Induction occurs over a period of days and is presumed to be due to an increase in the rates of enzyme synthesisS, 20. The dose of dexamethasone employed to produce PNMT stimulation has been very high, generally 0.5-1.0 mg/kg. The physiological role of glucocorticoids in the regulation of PNMT in the intact animal is less clear. Adrenal PNMT activity may be regulated by ACTH (indirectly acting through adrenal glucocorticoid synthesis), by circulating glucocorticoids directly, and also by neuronal activity via the splanchnic nerves in different strains of mice 5 and rats H. Short-term treatment with dexamethasone has been reported to be without effect on adrenal PNMT in the intact animaPg, z0, although the activity of the adrenal enzyme is increased 40 days after unilateral adrenalectomy 3 and the brain enzyme after 13 days of dexamethasone treatment lz. The half-life of adrenal PNMT, estimated without blockade of protein synthesis, is reported to be quite long (6 days) 4. Based on these considerations, Ciaranello and Black 4 have suggested that PNMT finds its bio- logical role only in chronic stress situations. Nothing is known regarding the effect of stress on the activity of PNMT in brain tissue. The neuroanatomical positions of the adrenergic cell bodies in the rostral medulla oblongata of the brain stem ~0 is suggestive of a relationship to stress. The ventral adren- ergic cell group (C1) coincides in part with the vasomotor center 9 and is thought to project to the spinal cord, the hypothalamus, and other forebrain regions known to mediate aspects of the stress response 10. The dorsal cell group (C2) is in part coincident with the cardioinhibitory center (the dorsal motor nucleus of the vagus) 9 which re- ceives input from baroreceptors.