Cardiac muscle Flashcards

1
Q

what is cardiac muscle composed of

A

cardiac myocytes (myocardial muscle cells) which are shorter, branched cells and usually contain a single nucleus.

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2
Q

what connects cardiac myocytes?

A

intercalated disks– composed of desmosomes and gap junctions

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3
Q

how do the t tubules in cardiac muscle compared to sk muscle?

A

fewer T tubs, but larger and wider t tubs

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4
Q

Smaller amounts of sarcoplasmic reCculum -cardiac muscle requires the entry of extracellular Ca2+
An abundance of mitochondria (~1/3 of cell volume) -oxidaCve metabolism for ATP producCon

A

ya

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5
Q

how is contraction initiated in myocytes?

A

not by neurons; generated by autorhythmic cells; depol starts at SA node; APs generated spontaneously

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6
Q

describe the AP pattern in autoryth cells

A

funny current channels open at -60 mV, net influx of Na; around -45 mV, some t-type Ca channels open and If channels close; at -40 mV, L-type Ca channels open; Ca induced Ca released– lots of L type channels open allowing for a sharp depol to +15 mV; Ca channels close, K opens–> efflux of K to -60 mV; then If channels open again, etc

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7
Q

why is the SA node the dominant pacemaker?

A

has lots of HCN channels so reaches threshold faster that the rest of network—>region with most HCN channels set HR

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8
Q

describe an AP in a myocardial cell

A

Ions that entered from an AP are transferred to adjacent cells through gap juncCons leading to depolarizaCon of the cell.

  • Once the adjacent cell reaches threshold voltage gated Na+ open causing the Na+ spike of acCon potenCal (green). (This AP also spreads to myocardial cells next to it through gap juncCons).
  • The posiCve voltage change of the AP slowly opens L-type Ca2+ channels. -There is a brief repolarizaCon from fast K+ channels (blue) before the Ca2+ influx through the L-type Ca2+ channels cause the K+ channels to close and lead to a sustained depolarizaCon (the plateau) (yellow)
  • once the Ca2+ channels close, slow K+ channels then open and hyperpolarize the cell (pink).
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9
Q

Excitation-contraction coupling in cardiac muscles

A

L-type Ca channels (DHP receptors) are not mechanically linked to RyR; depol flows through the membrane and causes Ca to enter through the L-type channels and bind to RyR on the SR to release more Ca–>sparks sum together–> this allows Ca to bind to sarcomeres; Ca-induced Ca released

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10
Q

relaxation in cardiac muscle

A

Ca unbinds from troponin; some Ca is pumped out into the ECF (moreso than in sk muscle) MOST of the Ca is taken back up into the SR

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11
Q

what regulates the SERCA pump?

A

PLN–PLN is active and activates the pump when phos;

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12
Q

how quicker relaxation(=quicker subsequent contraction) achieved?

A

reuptaking Ca faster

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13
Q

how is contractile force enhanced in cardiac muscle?

A

NOT through summation; in increase in ICF Ca in myocytes enhances contractile force;increased Ca2; length tension relationship

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14
Q

cardiac muscle is capable of graded single twitch contractions.

A

ya

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15
Q

how is contractile force enhanced in cardiac muscle through increased ICF Ca?

A

additional troponin complexes activated and

increased cross bridge formation leading to increased force of contraction

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16
Q

how is contractile force enhanced in cardiac muscle through length tension rlnshp?

A

cardiac muscle generates a higher force when slightly stretched

17
Q

what does the sympathetic NS affect in the heart?

A

increases HR/conduction velocity

affects autorhyth. cells and contractile cells

18
Q

how does the parasymp NS affect the heart?

A

decrease HR/conduction velocity– affects on autorhyth cells

19
Q

how does the symp NS modulate contraction?

A
  1. Phosphoryla5on of Ca2+ channels causes the calcium channels to remain open longer during ac5on poten5als.
  2. Phosphoryla5on of ryanodine receptors enhances sensi5vity to Ca2+, increasing release of Ca2+ from the sarcoplasmic re5culum.
  3. Phosphoryla5on of SERCA (PLN) increases the speed of Ca2+ re-uptake which increases Ca2+ storage
20
Q

explain the length tension rlnshp

A
  1. A slightly stretched sarcomere increases the Ca2+ sensi5vity of the
    myofilaments.
    -a stretched sarcomere has a decreased diameter which may reduce the distance that Ca2+ needs to diffuse increasing probability of cross-bridge cycling.
  2. A slightly stretched sarcomere puts addi5onal tension on stress- ac5vated Ca2+ channels, increasing Ca2+ entry from extracellular space and increasing Ca2+ induced Ca2+ release.
    when stretched, has a reduced diameter—>smaller distance of diffusion for Ca; more troponin complexes activated etc
21
Q

Parasympathe5c neurons containing ACh mainly innervate the SA and AV node influencing autorhythmic myocardial cells, decreasing the frequency of ac5on poten5als (decreasing heart rate).

A

ACh acts on muscarinic cholinergic receptors opening K+ channels and closing T-type Ca2+ channels and HCN channels.
-since the pacemaker ac5vity does not usually reside within the AV node, these mechanisms act at the AV node to decrease conduc5on velocity.

22
Q

Sympathe5c modula5on of pacemaker ac5vity

A

Beta1 adrenergic receptors can be ac5vated by NE released from sympathe5c neurons or epinephrine from the adrenal medulla

  • increase Na+ conductance through HCN channels: cells reach threshold more rapidly
  • increase Ca2+ conductance through Ca2+ channels:
  • cells reach threshold more rapidly, shorter dura5on AP
23
Q

what type of control is HR under?

A

tonic control

24
Q

what is tonic control?

A

never really rests? stays at RMP for long?