(a, b) In parallel experiments, normal A7r5 cells were treated with ionomycin and thapsigargin (I/Tg; 1 μM of each) to activate CCE causing an increase in Ba2+ (a) and Mn2+ (b) entry. Subsequent addition of AVP (100 nM) increased Ba2+ entry further, but inhibited Mn2+ entry, whether recorded using fluorescence excited at 340 or 360 nm. (c) AVP (100 nM) reversibly decreased the increase in [Ca2+]i evoked by CCE in normal A7r5 cells. (d) Even in cells lacking DAG lipase activity, arachidonic acid (20 μM) reversed the increase in [Ca2+]i evoked by CCE. (e) In normal cells, arachidonic acid (20 μM) inhibited Mn2+ entry via CCE. The persistent effect of arachidonic acid in these experiments (d, e), which occurred also in parallel measures of Sr2+ entry (results not shown), probably results from slow washout of arachidonic acid from the perfusion apparatus. Representative traces are shown, each typical of ≥3 (a–c) or 2 (d, e) similar experiments.