Haemodialysis acutely reduces the plasma levels of ADMA without reversing impaired NO-dependent vasodilation

End-stage renal disease patients have endothelial dysfunction and high plasma levels of ADMA (asymmetric ω-N^G,N^G-dimethylarginine), an endogenous inhibitor of NOS (NO synthase). The actual link between these abnormalities is controversial. Therefore, in the present study, we investigated whether HD (haemodialysis) has an acute impact on NO-dependent vasodilation and plasma ADMA in these patients. A total of 24 patients undergoing maintenance HD (HD group) and 24 age- and gender-matched healthy controls (Control group) were enrolled. The increase in forearm SkBF (skin blood flow) caused by local heating to 41 °C (SkBF41), known to depend on endothelial NO production, was determined with laser Doppler imaging. SkBF41 was expressed as a percentage of the vasodilatory reserve obtained from the maximal SkBF induced by local heating to 43 °C (independent of NO). In HD patients, SkBF41 was assessed on two successive HD sessions, once immediately before and once immediately after HD. Plasma ADMA was assayed simultaneously with MS/MS (tandem MS). In the Control group, SkBF41 was determined twice, on two different days, and plasma ADMA was assayed once. In HD patients, SkBF41 was identical before (82.2±13.1%) and after (82.7±12.4%) HD, but was lower than in controls (day 1, 89.6±6.1; day 2, 89.2±6.9%; P<0.01 compared with the HD group). In contrast, plasma ADMA was higher before (0.98±0.17 μmol/l) than after (0.58±0.10 μmol/l; P<0.01) HD. ADMA levels after HD did not differ from those obtained in controls (0.56±0.11 μmol/l). These findings show that HD patients have impaired NO-dependent vasodilation in forearm skin, an abnormality not acutely reversed by HD and not explained by ADMA accumulation.