Activation of TRPV4 or store-operated channels increases permeability in a Ca2+ entry-dependent fashion. In low (0.02 mmol/L) extracellular [Ca2+] (striped bars), Kf was measured at baseline (BL) and 45 min after treatment with the TRPV4 agonists 4αPDD or EETs or thapsigargin which activates store-operated channels. A final Kf was measured 15 min after Ca2+ add-back (2.2 mmol/L, closed bars). Vehicle (A) or the TRPV antagonist ruthenium red (1 μmol/L, panel B) was added 15 min prior to treatment. Ca2+ entry was required for the permeability response to all agonists (A), yet only the response to 4αPDD or EETs was blocked by ruthenium red (B). P values for ANOVA are shown above each group; post hoc tests identified specific differences: *p<0.05 vs. BL, #p<0.05 vs agonist in low Ca2+.