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. 2018 Mar 26;596(14):2663–2678. doi: 10.1113/JP275395

Figure 6. Exposure of pancreatic lobules to a mixture of POA and ethanol induces PSC responsiveness to trypsin.

Figure 6

In A and B, the effects of trypsin (50 nm) and BK (1 nm) on [Ca2+]i in PSCs in a control lobule are compared with those in lobules that had been exposed to a mixture of POA (20 μm) and ethanol (12 mm) for 2.5 h. In control PSCs, trypsin (50 nm) only evoked a Ca2+ signal in 2 cells out of 28 tested, and not in the case shown in A, whereas the same concentration of trypsin evoked a clear Ca2+ signal in the PSC in a lobule that had been treated with POA and ethanol (n = 14 out of 28 cells tested). C, summary of the results of the experiments illustrated in A and B, showing the marked increase in the percentage of PSCs responding to trypsin with Ca2+ signals after POA/ethanol exposure. In the presence of the CRAC channel inhibitor GSK‐7975A (20 μm), the percentage of PSCs responding to trypsin in the POA/ethanol groups was markedly reduced (n = 12 of 71 cells tested).