Absence of capsazepine effect on store-operated calcium entry (SOCE) in ASM cells in mouse PCLS. Mouse peripheral lung slices loaded with an intracellular calcium indicator dye were exposed to caffeine (20 mM) and ryanodine (25 μM) simultaneously to “lock” the ryanodine receptor of sarcoplasmic reticulum (SR) in the open state, to irreversibly deplete the SR of calcium, and to induce SOCE in the presence of zero-calcium external buffer. The slices were then reexposed to 1.3 mM Ca2+ extracellular buffer, and the resultant increase in ASM calcium-mediated fluorescence was considered a measure of SOCE. GSK 7575A, 100 µM, a SOCE inhibitor, significantly inhibited SOCE in this assay; however, 100 µM capsazepine did not. This suggests SOCE inhibition is not the mechanism by which capsazepine inhibits calcium oscillations in ASM. A: combined Ca2+-mediated fluorescent tracings. B: quantification of SOCE-mediate calcium influx. Values are means ± SE; n = 3. ***P < 0.001 and *P < 0.05 compared with untreated controls by ANOVA with Bonferroni post hoc correction.