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AP for Skeletal and Cardiac Myocytes
cardiac pacemaker cell has longer duration than skeletal muscle
cardiac contractile muscle has even longer duration
shape of cardiac contractile muscle graph could change depending on heart rate
membrane potential of the pacemaker cell does not remain constant at resting state after repolarization
Autorhythmic Cells
spontaneously generate action potentials
depolarization of the autorhythmic cells then spread rapidly to adjacent contractile cells through gap junctions
Autorhythmicity
refers to the combination of both the automaticity and rhythmicity properties
auto is to initiate own pace making activity
ryth is to maintain the regularity of pace making activity
membrane slowly depolarizes and drifts toward threshold between action potentials
pace maker cells exhibit the slow response in their action potentials
3 phases of the permeability changes for various ions are observed in the AP of the pacemaker cells
Phase 4 Autorhythmicity
gradual depolarization due to slow ionic influx creating funny current (If)
If is initiated by the opening of Na channels causing slow influx of Na into pacemaker cells through HCN channels which open during the end of repolarization
There are opening of transient Ca channels during the last half of the pacemaker potential that give rise to Ca influx
decays of K efflux due to closing of K channels towards end of repolarization
onset of pacemaker current
the net result is the resting membrane potential becomes progressively more positive for the pacemaker cells
Phase 0 Autorhythmicity
opening of the long-lasting voltage gated channels for Ca after reaching threshold (rapid influx of Ca)
depolarization occurs once the threshold potential is reached
no fast Na channel is involved, and the slope of the upstroke is not as steep as that of the AP for the contractile myocytes
Phase 3 Autorhythmicity
starts with the gradual closing of voltage gated Ca channels (Ca influx stops)
voltage gated K channels are now activated (rapid efflux)
repolarization occurs
once the membrane potential reaches the maximum diastolic potential, phase 4 will start again
Rate of Diastolic Depolarization
can influence cardiac rhythmicity
at phase 4
steeper slope will reach threshold quicker
norep. increases rate of diastolic depolarization which increases slope of phase 4 which increases heart rate
Maximum Diastolic Potential
can influence cardiac rhythmicity
induces hyperpolarization by K efflux
MDP becomes more negative, it needs a longer time to reach threshold potential, so heart rate decreases
Ach also decreases the slop of phase 4, further decreasing heart rate
Threshold Potential
can influence cardiac rhythmicity
quinidine
an antimalarial and antipyretic drug
shifts threshold voltage towards zero
takes longer time to reach the threshold potential, so decreased heart rate
Phase 0 Re/depolarization
rapid depolarization phase
occurs when the pacemaker potential spreads to the contractile myocytes and reaches the threshold of the contractile myocytes
triggers influx of Na through Na channels
Phase 1 Re/depolarization
early repolarization stage
rapid inactivation of the Na channels
together with the activation of the transient outward K current
brief efflux of K
Phase 2 Re/depolarization
plateau phase
so you can push blood out with adequate time
balance between K efflux and Ca influx
K efflux: through K channels known as delayed rectifier K channels
Ca influx: through long lasting Ca channels
Phase 3 Re/depolarization
repolarization
starts with inactivation of the L-type Ca channels
with the continuation on the efflux of K
inside the cell membrane becomes progressively more negative
cell is unexcitable during phases 0,1,2, and part of 3
Phase 4 Re/depolarization
restoration of ionic concentrations
concentration of Na and K return to their resting state by Na-K pumps
with 2 K entering and 3 Na leaving
Ca by both the Na-Ca exchangers and ATP driven Ca pumps