In response to a high sodium (Na + ) intake, salt-sensitive in salt-resistant (؉55 ؎ 16.0 ml/min/1.73 m 2 ) and saltsensitive patients (؉22 ؎ 21.5 ml/min/1.73 m 2 ). patients with hypertension retain more Na + and manifest a greater rise in arterial pressure than salt-resistant This study has shown that salt-sensitive AfricanAmericans manifest different systemic and renal patients. Because there is limited information regarding the role of nitric oxide (NO) in salt-sensitivity we examhaemodynamic responses to L-arginine than salt-resistant patients and controls. The fall in mean blood pressined the effects of L-arginine (500 mg/kg, i.v. for 30 min) on mean arterial pressure and renal haemodynamics in ure following L-arginine was greater in salt-sensitive than in salt-resistant patients and controls, whereas the 21 hypertensive and five normotensive African-Americans. At the end of L-arginine infusion mean arterial increase in ERPF was reduced in salt-sensitive compared to salt-resistant and normal subjects. The data are pressure fell more in salt-sensitive (−11.5 ؎ 2.5) than in salt-resistant (؊3.7 ؎ 1.5 mm Hg) and control subjects in keeping with the notion that a defect in NO production may participate to the genesis of blood pressure sensi-(؊3.2 ؎ 3.8 mm Hg). At the end of L-arginine infusion effective renal plasma flow (ERPF) increased more tivity to salt. (P Ͻ 0.05) in controls (+108 ؎ 13.9 ml/min/1.73 m 2 ) than