Ventricular Action

Potential

 The membrane potential is at -90mV due to K+

leaving the cell (through ungated channels,
constant process, dependent on the
concentration and has no change)
Na+ rushes out of the membrane at a fast rate
(rapid depolarization), [shown through the dip
down but is stopped because K+ is still leaving]
Due to Ca2+ going into cell a plateau occurs,
through L-type Calcium Channels. Calcium
channels shut off, only K+ leaves the membrane
therefore the interior becomes negative.

Phase 0
Fast Channels open, increasing the
conductance of Na+ Sodium influx
causes Depolarization
Channel open and closes quickly, and
have closed by the time the main
part of the plateau phase is entered

Phase 1
Slight repolarization is due to a
transient K+ current and closing of
the Sodium Channels

Phase 2
L-type Ca2+ channels open, conductance of Ca2+
increases, permitting Ca2+ influx
Voltage-gated K+ channels (iK1), are closed;
conductance of K+ decreases compare with resting
membrane
K+ efflux continues through the ungated K+
channels and possibly other channels
Development of the Plateau phase is dependent on
the closing of voltage-gated K+ channels
Calcium channel antagonist shorten the plateau
Potassium channel antagonists lengthen the plateau

Phase 3
L-type Ca2+ channels doses,
conductance of Ca decreases,
eliminating any influx through these
channels
Voltage-gated K+ channels, the
delayed rectifier iK, then the iK1 are
opened, increasing K conductance
Large potassium efflux begins, and
cell quickly repolarizes

Phase 4
Conductance of K+ is so high;
voltage- gated and ungated
potassium channels open. The
delayed rectifiers, iK, gradually
closes but are responsible for the
relative refractory period during
Phase 4