As in skeletal muscle and neuron, similarly in heart the depolarizing phase of action potential is mainly due to the opening of voltage-gated sodium channels. Sodium entry depolarizes the cell and sustain the opening of more sodium channel in positive feedback fusion. Unlike in other excitable tissue, in cardiac muscle the reduction in sodium permeability is not accompanied by membrane repolarization. The membrane remain depolarized at plateau of 0 mV.
The reason for continued polarization is potassium permeability stays below the resting value and a marked increase occurs in the membrane permeability to calcium. The original membrane depolarization causes voltage-gated calcium channels in the plasma membrane to open, which results in flow of calcium ions down their electrochemical gradient into the cell.
The channels open slower than sodium channel. They are L-type calcium channels because they remain open for prolonged period. Ultimately repolarization does occur when calcium channel slowly inactivate, and another subtype of potassium channel open.
SA node cell does not have steady resting potential, but instead undergo slow depolarization. This gradual depolarization is known as pacemaker potential. Three ion channel mechanism contribute to pacemaker potential. First is progressive reduction in potassium permeability. Potassium channel, which opened during the repolarization phase of previous action potential, gradually closes due to the membrane's return to negative potential. Second, pacemaker cells have unique set of channel that open when the membrane potential is at negative value. These non specific cation channel conduct mainly an inward, depolarizing sodium current by F-type sodium channel. The third pacemaker channel is a kind of calcium channel that opens only briefly but contributing an inward calcium current and an important final depolarizing boost to pacemaker potential by T-type calcium channels.
The reason for continued polarization is potassium permeability stays below the resting value and a marked increase occurs in the membrane permeability to calcium. The original membrane depolarization causes voltage-gated calcium channels in the plasma membrane to open, which results in flow of calcium ions down their electrochemical gradient into the cell.
The channels open slower than sodium channel. They are L-type calcium channels because they remain open for prolonged period. Ultimately repolarization does occur when calcium channel slowly inactivate, and another subtype of potassium channel open.
SA node cell does not have steady resting potential, but instead undergo slow depolarization. This gradual depolarization is known as pacemaker potential. Three ion channel mechanism contribute to pacemaker potential. First is progressive reduction in potassium permeability. Potassium channel, which opened during the repolarization phase of previous action potential, gradually closes due to the membrane's return to negative potential. Second, pacemaker cells have unique set of channel that open when the membrane potential is at negative value. These non specific cation channel conduct mainly an inward, depolarizing sodium current by F-type sodium channel. The third pacemaker channel is a kind of calcium channel that opens only briefly but contributing an inward calcium current and an important final depolarizing boost to pacemaker potential by T-type calcium channels.
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