excitation contraction coupling in cardiac myocytes. Flashcards

1
Q

myocyte

A

muscle cell

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2
Q

myocardium

A

muscle tissue

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3
Q

What are the 2 types of myocardium tissues?

A
  1. autorhythmic tissue

2. contractile myocardium

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4
Q

What does the autorhythmic myocardium tissue does?

A

its primary response is to generate heart rhythm. Action potentials are initiated here.
the autorhythmic myocardium (SA node) generates action potential without input from brain, these action potentials spontaneously depolarize in a set rhythm. They spread through contractile cells through gap junctions.

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5
Q

What does the contractile myocardium tissue do?

A

it contracts, shortens, and increase pressure on heart chambers.

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6
Q

Contractile myocardium structure:

A

intercalated disks connect cardiac muscles
gap junctions transfer depolarization between cells
no neuromuscular junctions, action potentials start int he cardiac conductor system.

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7
Q

Can chemical synapses generate rhythm?

A

No! but chemical synapses can modulate heart rhythm.

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8
Q

What 3 areas of the autorhythmic myocardium contain pacemaker cells that can spontaneously depolarize without any stimulus?

A
SA node (main 100 beats per minute)
Atrioventricular nodes (45 beats per minute)
Left and right Purkinjee fibers (45 to 25 beats per minutes)
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9
Q

Why is there a delay at the atrioventricular node?

A

The time it takes to depolarize the right atrium fully causes 100msec.

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10
Q

What is the passage of depolarization leading to contraction of the cardiac muscle?

A
  1. SA node depolarizes
  2. Electrical activity goes rapidly to AV node via internodal pathways
  3. Depolarization spreads more slowly across atria, conduction spreads through AV nodes.
  4. Depolarization moves rapidly through ventricular conducting system to the apex of the heart
  5. Depolarization wave moves upward through the apex.
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11
Q

How is action potential generated in the SA node and what are some exceptional points to take notes of ?

A

These cells have funny channels which allows spontaneous entry of Na+/K+ ions. Funny channels are triggered at hyperpolarizing state of -60mv. At this point a graded depolarization occur from a Net entry of Na+, higher driving force due to the electrical gradient. When this graded depolarization reaches the threshold, Ca2+ channels open and causes a net entry of Ca2+ and causes action potential. At the peak, K+ channels open and causes a rapid repolarization of the action potential. As the membrane reaches -60mv funny channels are triggered to open and another cycle of action potential generates.
Key notes:
1. No resting membrane potential.
2. Net entry of Na+ causes graded depolarization
3. Ca 2+ entry at threshold causes rapid firing of action potential
4. Negative feedback system
5. K+ leaving the cell repolarizes the cell membrane

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12
Q

How is action potential generated in cardiac muscle?

A

The action potential from the neighboring cell spreads through gap junction to the contractile muscle cells and causing a depolarization when voltage gated Na+ channels open. This leads to a net entry of Na+ due a higher driving force of Na+ electro gradient compared to K+. Na+ rapidly depolarizes the cell and the cell membrane reaches a potential of +20 mv. At that point Na+ inactivation gates close and there is an initial repolarization due a reduction of Na+ permeability. At this point, Ca2+ channels open, and the net influx of calcium channels flatten the depolarization creating the plateau phase. Ca2+ channels close and K+ channels open causing a K+ efflux and repolarize the cell to the resting membrane potential.
Key points:
1) There is a resting membrane potential and since it is equal to the equilibrium potential of K+ the cell never hyperpolarizes.
2. Ca2+ influx causes the plateau partially responsible is K+ fast channels closing.
3. Initial repolarization caused by the reduced permeability of Na+. (K+ is also leaving through K+ channels)

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13
Q

What is the refractory period and what is its role in cardiac muscles?

A

During refractory period a normal stimulus who would usually be able to excite the cell cannot fire another action potential. In cardiac muscles, the longer action potential prevents the summed contraction tetanus. In the refractory period the action potential is contained as long as the muscle is contracting, during this time no stimulus can generate a second action potential. During this refractory period, Na+ inactivation gates are kept closed.

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14
Q

What are the steps of cardiac excitation-contraction coupling?

A
  1. Action potential travels down the cell membrane, the depolarization is sensed by the DHP receptors.
  2. DHP receptors are calcium channels, so they open due to this voltage change and allow some calcium to enter the cell.
  3. Calcium binds to the RYR ligand gated channel* which releases calcium out of the SR.
  4. Calcium goes down its concentration gradient into the cytoplasm and binds to troponin.
  5. Tropomyosin shifts over and expose the actin-myosin binding site on the thin actin filaments.
  6. Myosin heads bind to actin, power stroke happens.
  7. for muscle relaxation, ca2+ is pumped into the SR by Ca2+ ATPase pump in the SR and the antiporter that takes Ca2+ out of the cell and lets Na+ inside the cell.
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