The nonmodulating trait thought to explain development of hypertension in 25 to 35% of patients, is characterized by abnormal angiotensin II (AII)-mediated control of aldosterone release and renal blood flow (RBF). Some data support the possibility that nonmodulation is an inherited trait, but others argue that it is an acquired epiphenomenon of the hypertensive state. We report the first case of a normotensive patient with nonmodulation who subsequently developed frank hypertension. Patient RR was studied on six occasions over a 5-year period, two while normotensive, four while hypertensive. This patient consistently demonstrated an abnormally low plasma aldosterone response to AII (3 ng/kg/min) on a low salt (10 mEq sodium) diet while both normotensive and hypertensive. A consistently abnormally depressed RBF response to AII on a high salt (150 to 200 mEq sodium) diet as well as a depressed RBF increment when the diet was changed from low salt to high salt were also noted. Thus, RR demonstrated nonmodulation by multiple criteria while both normotensive and hypertensive. We conclude that the nonmodulating trait may be a heritable defect that leads to the development of hypertension and is not an epiphenomenon.