ALTERED FLOW-DEPENDENT VASODILATATION OF CONDUIT ARTERIES IN MAINTENANCE HEMODIALYSIS

Background. An altered arterial nitric oxide (NO) pathway could partly explain the damage to arteries observed in haemodialyzed (HD) patient s. The present study was designed to non-invasively evaluate the NO pa thway of peripheral conduit arteries in HD patients. Methods. Twelve n ormotensive, non-diabetic HD patients treated with erythropoietin and 12 matched healthy controls (C) were included in the study. The effect of endogenous release of NO was assessed by measuring the flow-depend ent vasodilatation of the radial artery (post-ischaemic hyperaemia), a nd the response to exogenous NO assessed using sublingual glyceryl tri nitrate administration (GTN). Results. Radial artery diameter (echo-tr acking), radial blood flow (RBF: Doppler) and mean arterial pressure ( Finapres) were identical at baseline in HD patients and in healthy sub jects. The flow-dependent vasodilatation of the radial artery was decr eased in HD patients (C: 9+/-1% vs HD: 3+/-05%, P < 0.05). The decreas e in radial vascular resistance (C: -44+/-4% vs HD: -24+/-2%, P < 0.05 ) and the increase in radial diameter (C: 31+/-2% vs HD: 25+/-2%, P < 0.05) after GTN administration were less in HD patients than in contro ls. The ratio between the increase in diameter after hyperaemia to the increase in diameter after GTN, was also diminished in HD patients (C : 30+/-3% vs HD: 13+/-2%, P < 0.001). Conclusions. The flow-dependent vasodilatation of peripheral conduit arteries is altered in HD patient s and is associated with a slight but significant decrease in the vaso dilating response to exogenous NO. These results suggest, in the absen ce of changes in basal radial vascular resistance and arterial diamete r, more a decrease in endothelial NO bioavailability, than an increase in basal vascular tone.