Oral administration of L-arginine reduces intimal hyperplasia in balloon-injured rat carotid arteries.

Overview

Endogenous nitric oxide (NO) is produced from L-arginine by NO synthase. We evaluated the effect of oral administration of L-arginine on intimal hyperplasia in balloon-injured rat carotid arteries. Thirty Sprague-Dawley rats underwent balloon denudation on the left common carotid artery. Fifteen rats were treated with L-arginine in drinking water (2.5 mg/mL) two days before injury and were continued for 2 weeks. Another 15 rats served as controls. All animals survived without complications or body weight loss. In the treated group, daily intake of L-arginine was 170 +/- 43 mg/day. Plasma arginine levels were 130 +/- 32 micromol/L prior to L-arginine intake, 165 +/- 42 micromol/L at the day of injury, and 162 +/- 26 micromol/L at sacrifice. Intimal hyperplasia developed in all balloon-injured arteries in both control and L-arginine-treated animals. However, L-arginine-treated animals showed a 65% reduction of the intima/media area ratio and a 26% reduction of the intimal cell proliferation compared with control animals. These data indicate that adequate amounts of L-arginine were ingested by the rats and that oral administration of L-arginine significantly reduced intimal hyperplasia of balloon-injured arteries without any detectable toxicity.