Patient 1. A 46-year-old school teacher went to his family physician because of a nose bleed. He had suffered from frequent headaches for the previous 15 years and during the preceding 2 weeks had noticed an accentuation of his usual pain as well as progressive blurring of his vision. The physician documented the blood pressure at 260/150 mm Hg and admitted the patient to the regional hospital. On admission, the patient's blood pressure was 260/170 mm Hg; the heart rate was 90 beats/mm. He had no dyspnea. Auscultation disclosed an S3 gallop. In addition, he exhibited a grade-IV hypertensive retinop-athy with papilledema. Electrocardiogram revealed left ventricular hypertrophy. Laboratory tests revealed a serum creatinine of 119 mol/liter and proteinuria, 500 mg/24 hrs. Serum potassium and glucose were normal. Left ventricular hypertrophy was confirmed by a chest radiograph. The kidneys were normal in size and shape; computer-assisted tomography and renal arteriogram showed no abnormality. Initial therapy consisted of phentolamine and atenolol, which re-duced his blood pressure to 200/120 mm Hg. Six years ago, the patient was receiving captopril, 25 mg 3 times daily; minoxidil, 5 mg 3 times daily; atenolol, 100 mg/day; hydrochlorothiazide, 50 mg/day; and amiloride, 5 mg/day. He was referred to the Centre Hospitalier Universitaire Vaudois for management of his blood pressure. Two months after admission, he had stopped taking his minoxidil, and his blood pressure was 194/132 mm Hg. The serum creatinine increased transiently to 146 tmo1/liter but fell to 110 molIliter. The addition of furosemide, starting with 40 mg/day and increasing to 125 mg twice daily, induced a rebound of the serum creatinine level to 130 molfliter, but his blood pressure was 140/102 mm Hg 5 months after admission. Later, captopril was replaced by enalapril, 20 mg/day, and an attempt was made to reduce