We have determined that the adrenal glands of patients with the syndromes of low-renin essential hypertension and idiopathic hyperaldosteronism are abnormally sensitive to the steroidogenic effect of angiotensin II. The mechanism of this heightened responsiveness to angiotensin II is unknown but may be due to the bilateral adrenal hyperplasia present in many patients with these low-renin hypertension syndromes. We have found that metoclopramide, a dopamine antagonist, causes three-fold increases in levels of plasma aldosterone in normal subjects. These increases could not be accounted for by changes in plasma renin activity, ACTH or potassium. Metoclopramide does not stimulate bovine adrenal glomerulosa cells to produce aldosterone in vitro, suggesting that it stimulates the secretion of aldosterone in vivo indirectly, by increasing the levels or the activity of an undefined aldosterone stimulating factor. We have also found that human urine, after partial purification, stimulates bovine adrenal glomerulosa cells to produce aldosterone in vitro. Urine samples from patients with low-renin essential hypertension or idiopathic hyperaldosteronism have more stimulating activity than urine samples from normal subjects. These preliminary findings support the hypothesis that excessive production of an undefined aldosterone stimulating factor may be the basic abnormality in some cases of idiopathic hyperaldosteronism and low-renin essential hypertension.