Effect of L-arginine on acetylcholine-induced endothelium-dependent vasodilation differs between the coronary and forearm vasculatures in humans.

OBJECTIVES

The goal of this study was to determine whether the effect of L-arginine on endothelium-dependent vasodilation evoked with acetylcholine differs between the coronary and forearm vasculatures in humans.

BACKGROUND

Administration of L-arginine, a substrate in the production of endothelium-derived nitric oxide, may stimulate the release of nitric oxide.

METHODS

Seven patients with normal coronary angiograms and seven with mild coronary artery disease and hypertension underwent coronary arteriography and an intracoronary Doppler catheter technique, and the diameter of the large epicardial coronary artery and coronary blood flow were measured. Forearm blood flow was measured by use of a strain gauge plethysmograph.

RESULTS

Before L-arginine administration, acetylcholine (1 to 30 micrograms/min) increased coronary blood flow with modest vasoconstriction of a large coronary artery. Acetylcholine (4 to 24 micrograms/min) also increased forearm blood flow. The acetylcholine-induced increases in coronary and forearm blood flow were significantly less in patients with coronary artery disease than in control patients. Intracoronary infusion of L-arginine at 50 mg/min did not alter responses of the large coronary artery diameter or coronary blood flow to acetylcholine in either group. In contrast, L-arginine at 10 mg/min significantly (p < 0.01) augmented the forearm blood flow response to acetylcholine (4 to 24 micrograms/min) to a similar extent in the two groups.

CONCLUSIONS

The effect of L-arginine on acetylcholine-induced vasodilation differs between the coronary and forearm vasculatures in humans. It is suggested that impaired acetylcholine-induced coronary and forearm vasodilation in patients with coronary artery disease and hypertension may not be related to a limited availability of L-arginine.