Fig. 1.

Schematics illustrating the proposed hypothesis. A: action potential negatively polarized at virtual anode. B: depolarization at virtual cathode. Since Ca²⁺ equilibrium potential (E_Ca) is >60 mV, the driving force for Ca²⁺ entry through L-type Ca²⁺ channels is increased at virtual anodes but decreased at virtual cathodes. The increased Ca²⁺ entry triggers additional sarcoplasmic reticulum (SR) Ca²⁺ release, potentiating the intracellular Ca²⁺ concentration ([Ca²⁺]_i) transient selectively at virtual anodes but not at virtual cathodes. The potentiation of SR Ca²⁺ release at virtual anodes is also greater at longer stimulus (S₂) coupling intervals (a, b, and c in A and B) when SR Ca²⁺ release channels have had more time to recover from refractoriness. C: methods for measuring Δ[Ca²⁺]_i. The difference of the [Ca²⁺]_i amplitude (Δ) was measured 40 ms after the S₂.