Nitric oxide (NO) is synthesized from endothelium and has an important role in the control of vascular tonus. Adrenomedullin (AM) is a potent vasodilator, and cytoprotective peptide is produced not only in adrenal medulla, but also in the vascular smooth muscle and endothelial cells. To investigate the endothelial synthesis of AM and NO, and endothelial injury in Henoch-Schonlein purpura (HSP), we measured their levels in 16 children with HSP, who were evaluated during the acute and remission phases, and compared with 12 healthy controls. Plasma AM levels (pmol/ml) were significantly higher in acute phase children (46.87+/-11.49) than in those in remission (35.59+/-12.39, p<0.01) and controls (30.70+/-9.12, p<0.001). Similarly, plasma total nitrite levels (mumol/l) were higher in acute phase patients (47.50+/-12.30) than in those in remission (35.94+/-10.08, p<0.005) and controls (34.56+/-11.51, p<0.05). Urinary excretion of AM (pmol/mg creatinine) was higher in acute phase patients (53.85+/-23.22) than in remission patients (29.97+/-9.33, p<0.01) and controls (37.43+/-15.78, p<0.05). Patients had increased urinary nitrite excretion (mumol/mg creatinine) in acute phase (2.39+/-1.18) compared to those in remission (1.53+/-0.90, p<0.05) and controls (1.05+/-0.61, p<0.005). There was no significant difference between remission phase and controls in AM and nitrite levels (p>0.05). This study concluded that AM and NO may have a role in the immunoinflammatory process of HSP, especially in the active stage, although whether this perpetuates, or protects against, further vascular injury is not clear. Further studies are needed to clearly establish the roles of AM and NO in the pathogenesis of HSP.