Salt loading on plasma asymmetrical dimethylarginine and the protective role of potassium supplement in normotensive salt-sensitive Asians

Asymmetrical dimethylarginine (ADMA) is an endogenous inhibitor of NO synthase. Because endothelial NO pathway is compromised in patients with salt-sensitive hypertension, we investigated whether the plasma ADMA can be modulated by chronic salt loading in normotensive salt-sensitive persons and its relationship with NO, and we further determined whether or not dietary potassium supplementation can reverse them. Sixty normotensive subjects (aged 20 to 60 years) were selected from a rural community of Northern China. All of the people were sequentially maintained on a low-salt diet for 7 days Q g/day, NaCl), then a high-salt diet for 7 days (18 g/day), and high-salt diet with potassium supplementation for another 7 days (4.5 g/day, KCl). After salt loading, the plasma ADMA concentrations increased significantly in salt-sensitive subjects (0.89 +/- 0.02 mu mol/L versus 0.51 +/- 0.02 mu mol/L; P < 0.05), whereas the plasma NOx levels reduced considerably (41.8 +/- 2.1 mu mol/L versus 63.5 +/- 2.1 mu mol/L; P < 0.01). All of the abnormalities normalized when dietary potassium were supplemented (0.52 +/- 0.03 mu mol/L versus 0.89 +/- 0.02 mu mol/L for ADMA and 58.1 +/- 0.9 mu mol/L versus 41.8 +/- 2.1 mu mol/L for NOx). Statistically significant correlations were found among plasma ADMA level, the mean blood pressure, and the level of NO after salt loading in normotensive salt sensitive individuals. Our study indicates that high dietary potassium intake reduces blood pressure and ADMA levels while increasing NO bioactivity in normotensive salt-sensitive but not salt-resistant Asian subjects after salt loading.