Arterial compliance (AC) is an important determinant of vascular structure, and abnormalities of AC can greatly affect the cardiovascular system. Given the vasoconstrictive properties of increased levels of serum ionized calcium (iCa), we investigated the way that dialysate calcium level can influence AC in the hemodialysis (HD) population. In a crossover randomized design, 19 dialysis patients undergoing regular bicarbonate HD (three times weekly) underwent two cycles of four successive HD sessions each with a low (LdCa; 1.25 mmol/L) and high dialysate calcium concentration (HdCa; 1.75 mmol/L). At the fourth session of each cycle, iCa level and hemodynamic parameters (systolic blood pressure [SBP], diastolic blood pressure, mean arterial pressure [MAP], pulse pressure [PP], heart rate, and AC) were measured pre-HD and post-HD. AC was measured noninvasively at the brachial artery by arterial pulse waveform analysis. The dialysate calcium level was a significant determinant of both pre-HD (r = 0.335; P < 0.05) and post-HD iCa level (r = 0.767; P < 0.001). Pre-HD AC increased significantly (P < 0.05) by 0.01+/- 0.02 mL/mm Hg (7% +/- 19%) on switching from HdCa to LdCa treatment. Multiple regression analysis showed that both pre-HD PP and iCa level were major inverse determinants of pre-HD AC in both the LdCa (R(2) = 0.65; P < 0.001) and HdCa (R(2) = 0.51; P < 0.01) treatment groups. AC increased by 32% (P < 0.01) and 37% (P < 0.05) during LdCa and HdCa dialysis, respectively. Intradialytic changes in AC were inversely correlated with changes in SBP and PP. In the HdCa group, changes in iCa level related significantly to MAP (r = 0.464; P < 0.05). The results show that changes in AC during HD are mainly mediated through concurrent changes of systemic hemodynamics, which are largely affected by dialysate calcium level through parallel changes in iCa level. Interdialytically, a significant, blood pressure-independent, inverse relationship between AC and iCa level exists. Therefore, HD with LdCa, by reducing the incidence of HD-induced hypercalcemia, may have a beneficial role in preventing the ongoing reduction of AC in HD patients and thus improving cardiovascular prognosis.