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. Author manuscript; available in PMC: 2015 Aug 7.
Published in final edited form as: J Cell Physiol. 2015 Feb;230(2):337–346. doi: 10.1002/jcp.24709

Fig. 5.

Fig. 5

Ischemia-induced increase in ICl.Ca in mVMs was respectively inhibited by a specific pore-targeting anti-ANO1 antibody and T16Ainh-A01. ICl.Ca was recorded in mVMs respectively isolated from sham (A,a and B,a) and myocardial ischemic groups before (A,b and B,b) or after application of specific pore-targeting anti-ANO1 antibody and 30 µmol/L T16Ainh-A01 (A,c and B,c). (A,d and B,d) Summarized densities of ICl.Ca were plotted as a function of membrane potentials under given conditions; ICl.Ca was significantly up-regulated by myocardial ischemia and was dramatically inhibited by either specific pore-targeting anti-ANO1 antibody (n = 5) or T16Ainh-A01 (n = 5).