OBJECTIVE: To assess the effects of oral L-arginine supplementation on cutaneous vascular responses in patients with primary Raynaud's phenomenon (RP). METHODS: Double-blind, crossover comparison of placebo versus L-arginine (8 gm/day for 28 days). Cutaneous vascular responses in the fingers were assessed during iontophoresis of acetylcholine and sodium nitroprusside, which are endothelium-dependent and endothelium-independent vasodilators. RESULTS: In comparison with control subjects, patients with primary RP had diminished endothelium-dependent and -independent vasodilatation (P < 0.05, and P < 0.005, respectively, by analysis of variance). At the 3 doses used, vascular responses to acetylcholine were reduced by 71%, 64%, and 63%, respectively, and responses to sodium nitroprusside were reduced by 67%, 73%, and 66%, respectively. L-arginine had no significant effect on cutaneous vascular responses to acetylcholine or sodium nitroprusside in control subjects or patients with primary RP. CONCLUSION: Reduced vasodilator ability in primary RP is unlikely to be due to an impairment in the L-arginine/nitric oxide pathway.
RCT Entities:
OBJECTIVE: To assess the effects of oral L-arginine supplementation on cutaneous vascular responses in patients with primary Raynaud's phenomenon (RP). METHODS: Double-blind, crossover comparison of placebo versus L-arginine (8 gm/day for 28 days). Cutaneous vascular responses in the fingers were assessed during iontophoresis of acetylcholine and sodium nitroprusside, which are endothelium-dependent and endothelium-independent vasodilators. RESULTS: In comparison with control subjects, patients with primary RP had diminished endothelium-dependent and -independent vasodilatation (P < 0.05, and P < 0.005, respectively, by analysis of variance). At the 3 doses used, vascular responses to acetylcholine were reduced by 71%, 64%, and 63%, respectively, and responses to sodium nitroprusside were reduced by 67%, 73%, and 66%, respectively. L-arginine had no significant effect on cutaneous vascular responses to acetylcholine or sodium nitroprusside in control subjects or patients with primary RP. CONCLUSION: Reduced vasodilator ability in primary RP is unlikely to be due to an impairment in the L-arginine/nitric oxide pathway.