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. 2016 Jun 13;133(24):2348–2359. doi: 10.1161/CIRCULATIONAHA.116.021936

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© 2016 The Authors.

Circulation is published on behalf of the American Heart Association, Inc., by Wolters Kluwer. This is an open access article under the terms of the Creative Commons Attribution Non-Commercial-NoDervis License, which permits use, distribution, and reproduction in any medium, provided that the original work is properly cited, the use is noncommercial, and no modifications or adaptations are made.

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Figure 5. — Sarcoplasmic reticulum (SR) Ca²⁺ handling and high [Na⁺]_i in Purkinje cells (PCs). A, Representative traces of caffeine-induced Ca²⁺ transient from control ventricular myocytes (VMs; top left) and PCs (bottom left) and catecholaminergic polymorphic ventricular tachycardia VMs (top right) and PCs (bottom right) recorded at 3-Hz stimulation with 10 mmol/L caffeine. B, Mean peak SR Ca²⁺ content in each cell type. C, SR fractional release and (D) time to 50% decay from caffeine-induced Ca²⁺ transient VMs. E, Average NiCl₂-sensitive Na⁺/Ca²⁺ exchanger current/voltage relationships (voltage ramp protocol shown in the inset). F, Mean [Na⁺] concentration. *P<0.05.