EFFECTS OF L-ARGININE INFUSION ON RENAL HEMODYNAMICS IN PATIENTS WITHMILD ESSENTIAL-HYPERTENSION

Previous studies have shown that endothelium-derived relaxing factor/n itric 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 intra venous administration of L-arginine on blood pressure and renal hemody namics in 13 patients with mild essential hypertension and 15 normoten sive 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 mmHg i n hypertensive patients and from 106.1 +/- 3.0 to 97.5 +/- 2.9 mm Hg i n 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 su bjects, and glomerular filtration rate was unaffected in both groups. Although the L-arginine-induced reduction in mean blood pressure was s imilar in both groups, the decline in renovascular resistance was smal ler in hypertensive subjects. The response of renal plasma flow was al so smaller in hypertensive subjects. These findings suggest that dysfu nction of the L-arginine-nitric oxide pathway exists in the renal circ ulation even in mild essential hypertension with normal renal plasma f low and glomerular filtration rate. Thus, changes in renal endothelial function could be a cause rather than a consequence of hypertension.