1. Single oral doses (100, 200 and 300 mg) of moclobemide, a reversible inhibitor of monoamine oxidase (MAO) with predominant effects on the A‐ type of the enzyme, were administered to eight young, healthy male volunteers in a double‐blind, random‐order, placebo‐controlled study. The investigation was thereafter continued in an open fashion by administering a single 10 mg dose of the MAO‐B inhibitor deprenyl to the same subjects. 2. Deamination of catecholamines was powerfully and dose‐dependently inhibited by moclobemide, as evidenced by up to 40% decreases in the urinary excretion of deaminated catecholamine metabolites, corresponding increases in the excretion of non‐ deaminated, methylated metabolites, and up to 79% average decreases in the plasma concentration of 3,4‐dihydroxyphenylglycol (DHPG), a deaminated metabolite of noradrenaline (NA), and up to 75% average decreases in the plasma concentrations of 3,4‐dihydroxyphenylacetic acid (DOPAC), a deaminated metabolite of dopamine. The urinary excretion of 5‐hydroxyindoleacetic acid (5‐HIAA) was only slightly reduced. In contrast, deprenyl, in a dose which almost totally inhibited MAO‐B activity in blood platelets, did not appreciably affect the plasma concentrations of DHPG or DOPAC. 3. Due to the rapid, reversible, dose‐dependent and MAO‐A specific effect of moclobemide on plasma concentrations of DHPG, it is suggested that DHPG in plasma may be a useful indicator of the magnitude and duration of MAO‐A inhibition in man. 4. Sympatho‐adrenal function at rest was not significantly altered by moclobemide, as judged by unchanged plasma catecholamine concentrations and stable blood pressure and heart rate recordings. 5. Monoamine oxidase type B activity in blood platelets was slightly (less than 30%) and transiently inhibited after moclobemide. 6. The secretion of prolactin was dose‐dependently stimulated by moclobemide, whereas the plasma concentrations of growth hormone (hGH) and cortisol remained unchanged.