Background - Vascular nitric oxide (NO) bioavailability is reduced in patients with coronary artery disease (CAD). We investigated whether oral L- arginine, the substrate for NO synthesis, improves homeostatic functions of the vascular endothelium in patients maintained on appropriate medical therapy and thus might be useful as adjunctive therapy. Methods and Results - Thirty CAD patients (29 men; age, 67 ± 8 years) on appropriate medical management were randomly assigned to L-arginine (9 g) or placebo daily for 1 month, with crossover to the alternate therapy after 1 month off therapy, in a double-blind study. Nitrogen oxides in serum (as an index of endothelial NO release), flow-mediated brachial artery dilation (as an index of vascular NO bioactivity), and serum cell adhesion molecules (as an index of NO-regulated markers of inflammation) were measured at the end of each treatment period. L-Arginine significantly increased arginine levels in plasma (130 ± 53 versus 70 ± 17 μmol/L, P < 0.001) compared with placebo. However, there was no effect of L-arginine on nitrogen oxides (19.3 ± 7.9 versus 18.6 ± 6.7 μmol/L, P = 0.546), on flow-mediated dilation of the brachial artery (11.9 ± 6.3% versus 11.4 ± 7.9%, P = 0.742), or on the cell adhesion molecules E- selectin (47.8 ± 15.2 versus 47.2 ± 14.4 ng/mL, P = 0.601), intercellular adhesion molecule-1 (250 ± 57 versus 249 ± 57 ng/mL, P = 0.862), and vascular cell adhesion molecule-1 (567 ± 124 versus 574 ± 135 ng/mL, P = 0.473). Conclusions - Oral L-arginine therapy does not improve NO bioavailability in CAD patients on appropriate medical management and thus may not benefit this group of patients.
- Coronary disease
- Nitric oxide