Summary Unilateral renal hypertension was produced by constricting the aorta of the rat between the ostia of the main renal arteries. The acute stage of hypertension probably depended on a renal humoral mechanism since during the first 2 or 3 weeks of the hypertensive state, blood from the renal vein of the ischemic left kidney contained a potent vasoconstrictor substance, probably angiotensin, which was also present in arterial blood but not in renal vein blood from the untouched right kidney. After 3 weeks the left kidney ceased to release a pressor agent and in addition no such agent was demonstrable in the general circulation by bioassay. Hence the chronic stage of unilateral renal hypertension could not be attributed to the direct vasoconstructive effect of a humoral pressor agent.