Saralasin, 10 μg/kg per min, caused an immediate rise in blood pressure in 52 of 57(91.2%) hypertensive patients. The increase in diastolic pressure averaged 18.8 ± 1.83 mm Hg (mean ± SE) in normal renin patients on a normal salt intake. This immediate pressor response was absent in only five high renin patients and, conversely, was very large in three low renin patients. Direct arterial recordings are necessary to define the response accurately; it begins in 60-90 seconds, peaks in amplitude at 2.05 ± 0.38 minutes, and subsides over the next 5 minutes in normal renin and high renin patients. The blood pressure elevation is inversely related to background plasma renin activity (r = − 0.66,P< 0.001), and also is directly, but weakly, related to 24-hour urinary sodium excretion (r =+0.29). Therefore, the amplitude of the elevation is predictably diminished by the rise in plasma renin consequent to prior sodium restriction, and also by preliminary receptor exposure to low dose nonpressor infusions of saralasin itself (0.01-0.1 μg/kg per min). Phentolamine had no effect on the response in two patients. We propose that the immediate pressor response to saralasin is related directly to the preexisting degree of vacancy of angiotensin II vascular receptors and that the initial agonistic action of the drug may prove useful in defining the angiotensin II receptor status in hypertensive diseases.Circ Res44: 38-44,1979