Cardiac Muscle-Excitation and Signaling Flashcards
Why is cardiac contraction classified as myogenic?
it is not initiated by nervous input
What do we mean when we say the heart is a functional syncytium?
all myocardial cells are electrically connected to each other
T/F the heart can increase strength of contraction by recruiting more myocytes
F –> all or nothing tissue response (vs. skeletal muscle)
What mediates phase 0 of the cardiac action potential?
sodium channels (fast) –> sharp upstroke
What mediates phase 1 of the cardiac action potential?
efflux via transient K+ channels
What mediates phase 2 of the cardiac action potential?
influx of Ca2+ balanced by efflux of K+
What mediates phase 3 of the cardiac action potential?
K+ channels
What is the resting potential of cardiac myocytes?
approx -80mV (close to Ek)
What is the resting potential of cardiac SA/AV node?
no real resting potential but have diastolic depolarization causing pacemaker current
What is the myocyte membrane most permeable to at rest?
K+
What happens to Vr in a cardiac myocyte in a high [K+] solution?
higher resting potential AKA depolarized –> results in more Na+ channels being inactivated –> slower upstroke/phase 0
Describe the structure of the potassium channel.
four identical peptides with 6 transmembrane spanning helices each –> 5/6/P form the ion channel, 4 is the voltage sensor, P is the selectivity filter (GYG sequence)
What is the selectivity filter for the K+ channel?
GYG sequence –> P loop
What is the state of cardiac myocyte Na+ channels at rest?
almost all closed
What is the state of cardiac myocyte Na+ channels between -60 and -40 mV?
channels open
What is the state of cardiac myocyte Na+ channels after being open during a long pulse/sustained depolarization?
inactivated by ball/chain
If the window of voltage to have Na+ channels open but not inactivated is so small, how do we get physiologic action potentials?
inactivation occurs slower than channels are opened
The properties of the Na+ channel is blocked by what toxin?
tetrodotoxin
What is the role of T-type Ca2+ channels?
threshold/transient type calcium channels activate near the resting potential –> help with early depolarization (esp. in AV/SA nodes)
What is the role of L-type Ca2+ channels?
responsible for the plateau of phase 2 –> balance the efflux of K+ allowing for sustained depolarization –> activation/inactivation potentials are shifted to higher potentials (between -40 and 20 mV)
The properties of the T-type Ca2+ channel is blocked by what toxin?
amiloride
The properties of the L-type Ca2+ channel is blocked by what toxin?
D-600, Niphedipine
How do L-type Ca2+ channels extend the life of phase 2 plateau?
they inactivate very slowly
What is the role of inward rectifier K+ current?
responsible for resting potential (high conductivty at low potential: appears steeply sloped on I vs. V graph)–> switches off at -30mV aka when the heart is depolarized
*has a variable resistance hence the name rectifier
What is the role of delayed rectifier K+ current?
turns on very slowly –> responsible for repolarization after action potential
What are the effects that lead to repolarization of a myocyte after action potential?
slow inactivation of L-type calcium channels during the slow opening of delayed rectifier potassium channels followed by restoration of the inward rectifier potassium channel
What contributes to the slight repolarization during phase 1 of the cardiac action potential?
the rapid inactivation of T-type calcium channels during the slow activation of L-type calcium channels
T/F you need both Na and Ca channels to have cardiac action potentials
F –> either can start an AP but the shape will be different (e.g. without calcium channels there is no plateau)
Na or Ca channels? ventricular/atrial myocardium
Na current for conduction, CA current for plateau and activating contraction
Na or Ca channels? SA/AV nodes
Ca current for upstroke and propagation (Na current not active b/c resting potential is high enough to inactivate them)
Na or Ca channels? purkinje fibers/bundle of his
Na current for conduction, Ca current for plateau and slow responses when Na current is weak
What is the electrocardiographic representation of depolarization of the ventricles?
QRS
What is the electrocardiographic representation of repolarization of the ventricles?
t wave
What is the electrocardiographic representation relates to the length of the ventricular cardiac action potential?
time lag between Q and T aka QT
What can contribute to long QT syndrome?
genetic or drug induced: blockage of delayed rectifier K+ channels or excess Na channels
What are the dangerous consequences of long QT syndrome?
secondary after depolarizations leading to possible cardiac arrhythmia
How do the APs of ventricular and atrial myocardium differ?
atrial myocardium has a faster/steeper plateau
How do the APs of SA node and bundle fibers differ?
SA node has no resting potential but rather has diastolic depolarization, bundle fibers have a prominent phase 1 repolarization and a negative plateau
How do the APs of SA node and AV node differ?
AV node is slower –> delay allows for ventricular filling
Are purkinje fibers nerves or myocytes?
myocytes with mild contractile ability
What current contributes to the diastolic depolarization of pacemaker potentials?
funny current (If)serves as the bridge between inactivating delayed rectifier K+ channels (Ik) (inactivation leads to an initial depolarization) and the transient calcium current (Ica) that controls the pacemaker upstroke
What is the directionality of If?
inward current (potassium and sodium in some funky combination) depolarizes the cell
How many connexins form a connexon?
6
What ion is the major source of current flow between cardiac myocytes?
potassium
What ions are the major source of return current flow as action potentials propagate through cardiac myocytes?
sodium and chloride in the extracellular space –> contributes to voltage measured by EKG
