In 40-50% of patients with essential hypertension, a high sodium intake does not increase renal blood flow (RBF). These patients have been defined as nonmodulators because sodium intake does not modulate renal and adrenal responsiveness to angiotensin II (All). To define the role of All in mediating this altered responsiveness, we assessed the effect of a converting enzyme inhibitor (enalapril) on RBF and its responsiveness to All in 25 patients with essential hypertension-10 modulators and 15 nonmodulators-and 9 normotensive controls. After 5 d of a 200-meq sodium intake, the nonmodulators did not increase RBF, whereas the normotensives (79±28 ml/ min per 1.73 m2) and modulators (75±26 ml/min per 1.73 in2) did (P < 0.025). Arterial blood pressure did not change in the modulators with the salt loading, whereas in the nonmodulators, blood pressure rose (P < 0.004).After enalapril administration for 66 h, there was a significant difference (P < 0.01, Fisher Exact Test) in the blood pressure response in the two hypertensive subgroups. In the modulators, there was no change; in the nonmodulators, despite the high salt diet, a blood pressure reduction occurred. In parallel, basal RBF and RBF responsiveness to All were not changed after converting enzyme inhibition in the normotensive control (n = 9) or the hypertensive modulators (n = 10). Conversely, in the nonmodulators (n = 14), the basal RBF increased significantly (83±25 ml/min per 1.73 M2; P = 0.01), the increment being indistinguishable from the response to salt loading in normal subjects. Furthermore, renovascular responsiveness to infused All was also significantly enhanced (P = 0.027) in the nonmodulators, suggesting that enalaprilinduced increase in RBF reflected a fall in intrarenal All levels, and not an increase in prostaglandins or kinins, which would have blunted the renal response to All.Thus, short-term converting enzyme inhibition corrected abnormalities in sodium-mediated modulation of renal vascular responsiveness to All. The close quantitative relation of the increase in RBF with sodium loading in normal subjects and modulators, and with converting enzyme inhibition in nonmodulators, viewed in the context of the effectiveness of enalapril only in the latter, and parallel shifts in sensitivity to All, raises the intriguing possibility that converting enzyme inhibition reversed the failure of the renal blood supply to respond to