3.6 - Cardiac Muscle Flashcards

1
Q

What do “myo” and “cardiac” mean literally?

A
myo = muscle
cardiac = heart
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2
Q

Cardiac muscle cells are called:

A

myocardial cells

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3
Q

TRUE OR FALSE:

Myocardial cells are not striated

A

FALSE

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4
Q

Are myocardial cells organized in sarcomeres?

A

Yes

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5
Q

How do cardiac muscle cells differ from skeletal muscle cells?

A
  • much smaller with single nucleus with about 1/3 cell volume occupied by mitochondria
  • T tubules are larger and branched
  • SR is smaller
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6
Q

How are adjacent cells joined?

A

intercalated discs with desmosomes

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7
Q

What do desmosomes do?

A

transmit force from one cell to another

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8
Q

what are auto rhythmic cells and what do they do?

A
  • electrical conducting system of the heart
  • initiate the heart beat, spread electrical excitation rapidly throughout the heart
  • connected to other cardiac cells via gap junction
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9
Q

steps of cardiac muscle contraction:

A
  • action potential enters from adjacent cell
  • voltage gated Ca2+ channels open, Ca2+ enters cell
  • Ca2+ induces Ca2+ release through RyR channels on SR (90% of Ca2+ needed for contraction)
  • local release causes Ca2+ spark
  • summed Ca2+ sparks create Ca2+ signal
  • Ca2+ ions bind to troponin to initiate contraction
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10
Q

What type of contraction is exhibited by cardiac cells? Explain

A

graded contraction;-

  • force generated is proportional to number of active crossbridges
  • number of active crossbridges is proportional to cytosolic Ca2+ concentrations
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11
Q

What factors influence cardiac muscle contraction force?

A

i) changes in [Ca2+] :
- regulated by epinephrine and norepinephrine –> bind to and activate b1 Adrenergic receptors
- binding activates cAMP second messenger signalling pathway which leads to:
phosphorylation of voltage gated Ca2+ channels, increasing probability of channel to open to Ca2+
phosphorylation of phospholamban
- leads to increase SR Ca2+ - atpASE activity –> increase SR Ca2+
ii) Sarcomere length:
- tension generated is proportional to length of muscle fibre
- due to degree of overlap between actin and myosin
- stretching myocardial muscle cell may allow more ca2+ to enter through cell membrane ca2+ channels

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12
Q

The cardiac muscle is an excitable, this means it can

A

generate action potentials

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13
Q

list the major sequence of events:

A

phase 4: resting membrane potential (around 90mV)
phase 0: depolarization: AP opens voltage gated Na+ channels, causing a rapid increase in membrane Na+ permeability (close again)
phase 1: initial repolarization: open fast k+ channels allow initial repol
phase 2: plateau: initial depolarization triggered voltage gated ca2+ channels to slowly open, causing increase in Ca2+ permeability and fast K+ channels close
phase 3: rapid repolarization: ca2+ channels close and slow voltage gated k+ channels open (initial depolarization was the trigger), resting stage ion permeability is restored (phase 4)

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14
Q

The sustained depolarization is due to what?

A

slow opening of voltage gated Ca2+ channels

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15
Q

What are the results of sustained depolarization?

A

typical AP in cardiac muscle takes longer (around 200 msec) vs. 1-5 msec in neuron or skeletal muscle

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16
Q

Why is it important for cardiac muscles to have longer AP?

A

allows the heart to relax between contractions and prevents tetanus as it has to last for a while

17
Q

Why don’t cardiac muscle cells undergo summation and tetanus?

A

because of the longer refractory period, the cell has finished contracting before the next action potential