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. 2017 Jul 19;7:5895. doi: 10.1038/s41598-017-06247-3

Figure 4.

Figure 4

Activation of TRPC3 channels protects IKCa and SKCa channels from H-R-induced inhibition in PCAECs. (a) Representative traces and current-voltage relationship of whole-cell K+ current in PCAECs from different treatment groups before and after bradykinin (BK) stimulation with further application of the IKCa channel blocker TRAM-34 and the SKCa channel blocker apamin. Under H-R condition, PCAECs treated with OAG shows enhanced basal and BK-induced K+ currents compared with the cells without OAG-treatment and such enhancement is diminished by Pyr3. *p < 0.05, **p < 0.01, BK vs. basal; #p < 0.05, ##p < 0.01, BK + TRAM-34 vs. BK; ^p < 0.05, ^^p < 0.01, BK + TRAM-34 + Apamin vs. BK + TRAM-34. (b) Summarized data of BK-induced IKCa and SKCa currents from 5 independent experiments, each obtained from cell isolates of different hearts. PCAECs were subjected to H-R exposure in the absence or presence of the TRPC3/6/7 activator OAG before patch-clamp recording. For cells subjected to H-R exposure and OAG treatment, the current recording was performed under the condition without (H-R + OAG-treated) or with Pyr3 application (H-R + OAG-treated + Pyr3). *p < 0.05, **p < 0.01; one-way ANOVA and Scheffe post-hoc test.