Effect of L-arginine on systemic and renal haemodynamics in salt-sensitive patients with essential hypertension

In response to a high sodium (Na+) intake, salt-sensitive patients with hypertension retain more Na+ and manifest a greater rise in arterial pressure than salt-resistant patients. Because there is limited information regarding the role of nitric oxide (NO) in salt-sensitivity we examined the effects of L-arginine (500 mg/kg, i.v. for 30 min) on mean arterial pressure and renal haemodynamics in 21 hypertensive and five normotensive African–Americans. At the end of L-arginine infusion mean arterial pressure fell more in salt-sensitive (−11.5 ± 2.5) than in salt-resistant (−3.7 ± 1.5 mm Hg) and control subjects (−3.2 ± 3.8 mm Hg). At the end of L-arginine infusion effective renal plasma flow (ERPF) increased more (P < 0.05) in controls (+108 ± 13.9 ml/min/1.73 m2) than in salt-resistant (+55 ± 16.0 ml/min/1.73 m2) and salt-sensitive patients (+22 ± 21.5 ml/min/1.73 m2).This study has shown that salt-sensitive African–Americans manifest different systemic and renal haemodynamic responses to L-arginine than salt-resistant patients and controls. The fall in mean blood pressure following L-arginine was greater in salt-sensitive than in salt-resistant patients and controls, whereas the increase in ERPF was reduced in salt-sensitive compared to salt-resistant and normal subjects. The data are in keeping with the notion that a defect in NO production may participate to the genesis of blood pressure sensitivity to salt.