L-type channel is described as

L-type channel is described as

• A. Fast inward, short current; phase 2 of non-pacemaker AP
• B. Slow inward, long-lasting current; phase 2 of non-pacemaker AP and late phase 4 and phase 0 of SA/AV nodal cells
• C. Transient outward current in nodal cells
• D. Activated by acetylcholine

Answer: (B)

L-type calcium channels are high-threshold, long-lasting calcium channels that produce a slow inward current. In non-pacemaker myocardium, this Ca2+ influx sustains the plateau phase (phase 2) of the action potential, keeping the cell depolarized for a brief period. In SA and AV nodal tissue, the upstroke (phase 0) is driven by calcium entry through these same L-type channels rather than by sodium, and they also contribute as the cell approaches threshold during late phase 4, helping to set the pace. That combination—slow inward, long-lasting Ca2+ current with a major role in phase 2 of the non-pacemaker AP and in late phase 4 and phase 0 of nodal cells—accurately describes the L-type calcium current. It is not the transient outward current (Ito) and it is not activated by acetylcholine; acetylcholine acts via GIRK channels to hyperpolarize rather than activate L-type Ca2+ channels.

L-type calcium channels are high-threshold, long-lasting calcium channels that produce a slow inward current. In non-pacemaker myocardium, this Ca2+ influx sustains the plateau phase (phase 2) of the action potential, keeping the cell depolarized for a brief period. In SA and AV nodal tissue, the upstroke (phase 0) is driven by calcium entry through these same L-type channels rather than by sodium, and they also contribute as the cell approaches threshold during late phase 4, helping to set the pace. That combination—slow inward, long-lasting Ca2+ current with a major role in phase 2 of the non-pacemaker AP and in late phase 4 and phase 0 of nodal cells—accurately describes the L-type calcium current. It is not the transient outward current (Ito) and it is not activated by acetylcholine; acetylcholine acts via GIRK channels to hyperpolarize rather than activate L-type Ca2+ channels.