Effects of L-arginine on forearm vessels and responses to acetylcholine

This study was designed to investigate the effects of L-arginine (the substrate of endothelium-derived nitric oxide) in human forearm vessels. We examined whether intra-arterial infusion of L-arginine dilated forearm vessels and augmented vasodilatory responses to acetylcholine in young, healthy humans. The left brachial artery was cannulated for drug infusions and direct measurement of arterial pressure. Forearm blood flow was measured by a strain gauge plethysmograph. Intra-arterial infusions of L-arginine at 10, 20, 40, and 60 mg/min increased forearm blood flow from 4.7±0.6 to 4.9±0.5, 5.7±0.5, 7.2±0.8, and 8.2±0.9 ml · min^-1 · 100 ml^-1, respectively (n=8, p<0.01), whereas D-arginine at the same doses did not alter forearm blood flow (n=7). Intra-arterial infusions of acetylcholine (n=7) (4, 8, 16, and 24 μg/min) and sodium nitroprusside (n=5) (0.2, 0.4, 0.8, and 1.2 μg/min) increased forearm blood flow dose dependently (p<0.01 for both). Arterial pressure was not altered with infusions of these drugs. Responses to acetylcholine were augmented with simultaneous intra-arterial infusion of L-arginine at 10 mg/ml (p<0.01) but not with D-arginine. Responses to sodium nitroprusside were not altered by L-arginine. These results in human forearm resistance vessels support the notion that vasodilation induced by acetylcholine is a result of the conversion from L-arginine to endothelium-derived nitric oxide. Our results suggest that intra-arterial infusion of L-arginine may facilitate production of nitric oxide in the forearm and that L-arginine contributes to the modulation of vascular smooth muscle tone in healthy humans.