title: Haemodialysis acutely reduces the plasma levels of ADMA without reversing impaired NO-dependent vasodilation.
abstract: End-stage renal disease patients have endothelial dysfunction and high plasma levels of ADMA (asymmetric omega-NG,NG-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 degrees 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 degrees 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 micromol/l) than after (0.58+/-0.10 micromol/l; P<0.01) HD. ADMA levels after HD did not differ from those obtained in controls (0.56+/-0.11 micromol/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.
authors.affiliation: Division de Physiopathologie Clinique, Centre Hospitalier Universitaire Vaudois et Université de Lausanne, BH10-701 Lausanne, Switzerland.
authors.forename: Rolf P
authors.initials: RP
authors.lastname: Engelberger
authors.forename: Daniel
authors.initials: D
authors.lastname: Teta
authors.forename: Hughes
authors.initials: H
authors.lastname: Henry
authors.forename: Olivier
authors.initials: O
authors.lastname: De Senarclens
authors.forename: Benoît
authors.initials: B
authors.lastname: Dischl
authors.forename: Lucas
authors.initials: L
authors.lastname: Liaudet
authors.forename: Michel
authors.initials: M
authors.lastname: Burnier
authors.forename: Bernard
authors.initials: B
authors.lastname: Waeber
authors.forename: François
authors.initials: F
authors.lastname: Feihl
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D001120:Arginine / Q000031:analogs & derivatives* / Q000097:blood; D016022:Case-Control Studies; D004730:Endothelium, Vascular / Q000503:physiopathology; D005260:Female; D006801:Humans; D007676:Kidney Failure, Chronic / Q000097:blood / Q000503:physiopathology / Q000628:therapy*; D008297:Male; D008875:Middle Aged; D009569:Nitric Oxide / Q000502:physiology*; D012039:Regional Blood Flow / Q000502:physiology; D006435:Renal Dialysis; D012867:Skin / Q000098:blood supply; D012881:Skin Temperature / Q000502:physiology; D014664:Vasodilation / Q000502:physiology*
chemical_list: D009569:Nitric Oxide; C024917:symmetric dimethylarginine; D001120:Arginine