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Ventricular Action Potential

Action Potantial

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Action potential

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Page 1: Action Potantial

Ventricular Action Potential

Page 2: Action Potantial

• 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.

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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

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Phase 1

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

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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

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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

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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