L-arginine increases exercise-induced vasodilation of the forearm in patients with heart failure.

To determine whether L-arginine, a precursor of nitric oxide, can improve exercise-induced vasodilation of the forearm in patients with heart failure, we measured forearm blood flow in 9 patients with heart failure and in 7 age-matched control subjects before and after intra-arterial infusion of L-arginine. Resting forearm blood flow was significantly lower in patients with heart failure than in control subjects (2.34 +/- 0.85 (SD) vs 4.76 +/- 0.77 ml/min per 100 ml, p < 0.001). Endothelium-dependent vasodilation induced by acetylcholine was attenuated in patients with heart failure (p < 0.05). Exercise-induced vasodilation after handgrip exercise was significantly lower in patients with heart failure (p < 0.05). Intra-arterial infusion of L-arginine did not change basal forearm blood flow but significantly augmented acetylcholine-induced vasodilation in both patients with heart failure and control subjects (p < 0.05). Although L-arginine did not affect maximum forearm blood flow after handgrip exercise in control subjects (before, 26.2 +/- 13.5; after, 25.7 +/- 14.3; p = NS), it was increased in patients with heart failure (from 15.2 +/- 4.9 to 24.7 +/- 14.6, p < 0.01). The finding that L-arginine increased both acetylcholine- and exercise-induced vasodilation in patients with heart failure suggests that endothelial dysfunction might play an important role in impaired exercise-induced vasodilation in patients with heart failure.