Effects of l -Arginine Infusion on Renal Hemodynamics in Patients With Mild Essential Hypertension

Abstract

Abstract Previous studies have shown that endothelium-derived relaxing factor/nitric oxide plays an important role in the regulation of systemic and renal hemodynamics. The purpose of the present study was to determine whether endothelium-dependent renovascular relaxation was impaired in patients with mild essential hypertension who had normal renal plasma flow and glomerular filtration rate. We evaluated the effects of intravenous administration of l -arginine on blood pressure and renal hemodynamics in 13 patients with mild essential hypertension and 15 normotensive control subjects. l -Arginine infusion (500 mg/kg over 30 minutes) reduced mean blood pressure (from 82.5±2.5 to 76.3±2.6 mm Hg in hypertensive patients and from 106.1±3.0 to 97.5±2.9 mm Hg in control subjects; P <.001) and renovascular resistance (from 0.084±0.009 to 0.067±0.009 mm Hg · mL −1 · min −1 · [1.48 m 2 ] −1 and from 0.105±0.010 to 0.093±0.011 mm Hg · mL −1 · min −1 · [1.48 m 2 ] −1 , respectively; P <.001). l -Arginine infusion increased renal plasma flow (from 602±36 to 698±40 mL · min −1 · [1.48 m 2 ] −1 , P <.05) in normotensive subjects but not in hypertensive subjects, and glomerular filtration rate was unaffected in both groups. Although the l -arginine–induced reduction in mean blood pressure was similar in both groups, the decline in renovascular resistance was smaller in hypertensive subjects. The response of renal plasma flow was also smaller in hypertensive subjects. These findings suggest that dysfunction of the l -arginine–nitric oxide pathway exists in the renal circulation even in mild essential hypertension with normal renal plasma flow and glomerular filtration rate. Thus, changes in renal endothelial function could be a cause rather than a consequence of hypertension.