Plasma renin levels are elevated in accelerated or malignant hypertension. To see if this increase of renin is a concurrent phenomenon or a pathogenetic factor in the increase of blood pressure, severe hypertension was produced in rats by occluding the aorta between the origins of the renal arteries. Eight days later, these animals had developed severe hypertension (mean blood pressure = 201 ± 3 mm Hg) and markedly elevated plasma renin levels (151 ± 35 ng angiotensin II/ml hr -1 ; normal range = 11 ± 0.6). When the kidney distal to the ligature was excised at the time of the coarctation, the animals developed only a moderate increase in blood pressure (mean = 120 ± 1.3 mm Hg) and their plasma renin levels remained in the normal range. When the nonnephrectomized animals with severe hypertension were injected with antibodies against angiotensin II, blood pressure decreased, reaching its lowest point (126 ± 12 mm Hg) 2 days later. This work demonstrates that the severe increase in blood pressure is not due to the mechanical increase in resistance caused by complete coarctation of the aorta; rather, it is due to a humoral factor produced by the kidney, and this factor is renin.