Incubated capsular adrenal glands (»zona glomerulosa«) of potassiumdeficient rats converted approximately 30 times less tritiated corticosterone to aldosterone and 18-hydroxycorticosterone than capsular adrenals of potassium-replete rats. This difference was demonstrable over a large range of substrate concentrations. Capsular adrenal mitochondria of potassium-deficient rats also incorporated considerably less tritiated corticosterone into aldosterone and 18-hydroxycorticosterone than mitochondria of potassium-replete rats. Conversion to both corticosteroid fractions increased within 4 hours and became normal within 24 hours of resumed potassium intake. On the other hand, potassium intake only marginally affected the ratio of 18-hydroxycorticosterone formation to aldosterone formation by capsular adrenals and had no effect on the conversion of tritiated deoxycorticosterone to 18-hydroxydeoxycorticosterone and 18-hydroxycorticosterone by decapsulated adrenals (»zona fasciculata-reticularis« These findings indicate that potassium intake enhances 18-hydroxylase activity selectively in the zona glomerulosa of the rat adrenal cortex, but yield no information concerning an effect on 18-hydroxydehydrogenase activity. Kinetic data suggest that the potassium-induced increase in 18-hydroxylase activity is most likely due to de novo enzyme synthesis.