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Lecture

BIOC63H3 Lecture Notes - Cardiac Muscle, Threshold Potential, Membrane Potential


Department
Biological Sciences
Course Code
BIOC63H3
Professor
Ivana Stehlik

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Cardiovascular system: The Heart
Electrophysiology of Cardiac Muscle and the Origin of the Heart Beat
An action potential (AP) is the transient depolarization of a cell as a result of activity of ion
channels. The cardiac AP is considerably longer than those occurring in nerve or skeletal muscle
(~300 ms vs. ~ 1-3 ms). This is due to the presence of a plateau phase in cardiac muscle, which
lasts for 200-300 msec.
Ventricular muscle action potential (Figure 1a and Figure 2)
Initiation of the action potential
At rest, the membrane is most permeable to K+ and the resting potential is primarily dependent
on the K+ concentration gradient. An AP is initiated when the membrane is depolarized to a
threshold potential (~ - 55 mV). The initial depolarization results from transmission from an
adjacent cell through intercalated disks (Figure 4). At the threshold potential the inward
current caused by entry of Na+ through voltage-gated Na+ channels (INa) becomes large enough
to overcome the outward current through K+ channels, and thus causes further depolarization.
This in turn activates more Na+ channels. The depolarization thus becomes self-generating, and
so results in a very rapid upstroke (phase 0). At this point the membrane is more permeable to
Na+ than K+ because of the open Na+ channels. The Na+ concentration gradient therefore
becoming the major determinant of membrane potential and the cell moves towards the
equilibrium potential for Na+ (~+65 mV). It does not reach this potential both because it is
limited by the existing K+ permeability, and because of rapid inactivation (shutting) of the Na+
channels. The Na+ channels cannot be reactivated until the potential becomes more negative
than ~ 55 mV. Therefore another AP cannot be initiated until the cell repolarizes to at lesat this
potential (absolute refractory period). At slightly more negative potentials some Na+ channels
reactivate, allowing an AP to be initiated by a sufficiently large stimulus (relative refractory
period). All Na+ channels are reactivated by the time the cell is completely repolarized. The
refractory period, and the length of the AP compared to the twitch means that, unlike skeleton
muscle, cardiac muscle cannot be tetanized (Figure 1c).
The plateau phase
At the end of the upstroke, membrane Na+ permeability returns to its resisting valve, and in
skeleton muscle this results in rapid repolarization. In cardiac muscle however, the membrane
potential decays slowly over ~ 250 ms before a more rapid repolarization phase. This period of
slow decay is the plateau phase (phase 2), and is primarily due to Ca2+ current entering the cell
via voltage-sensitive L-type Ca2+ channels which activate relatively slowly when the membrane
potential becomes positive than -35mV. The
Resultant Ca2+ current (slow inward current or ISI), coupled with a reduced K+ outward
current, is sufficient to slow repolarization until the potential falls to ~ - 20 mV. The length of
the plateau is related to slow inactivation of Ca2+ channels. Ca2+ entry during the plateau is
vital for contraction; blockers of L-types of Ca2+ channels (example, dihydropyridines) reduce
force.

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