The effects of acute hypercalcemia on renal hemodynamics and renal autoregulation were evaluated in anesthetized mongrel dogs. Calcium concentration was increased by infusion of an isotonic calcium chloride solution (100 mM Ca2+) intravenously at 2 different rates. At the lower rate of infusion (0.65 ml/min), the plasma ultrafilterable calcium concentration [UF(Ca)] increased from 2.47 ± 0.16 to 3.46 ± 0.17 meq/l; the ultrafilterable calcium fraction decreased from 58 ± 3 to 53 ± 3%. Renal vascular resistance (RVR) increased slightly (14%) in association with small decrements in renal blood flow (RBF) and glomerular filtration rate (GFR). Calcium excretion rate increased by 147%, due primarily to a depression of fractional reabsorption from 99.1% to 98.06%. During the higher rate of infusion, UF(Ca) increased further to 4.0 ± 0.19 and 4.5 ± 0.2 meq/l, and was accompanied by proportionately greater effects on RBF and GFR, indicating a nonlinear relationship between these variables and UF(Ca). Calcium excretion was augmented markedly due to progressive depressions in fractional calcium reabsorption at all levels of UF(Ca) evaluated. The ability of the renal vasculature to autoregulate in response to decreases in renal arterial pressure was maintained with a high degree of efficiency during hypercalcemia. Changes in filtered calcium load were variable, depending on whether the increase in UF(Ca) or the decrease in GFR predominated. However, the depression of fractional calcium reabsorption was associated specifically with the increase in UF(Ca) and not the relative change in filtered calcium load.