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ESA 2- Cardiovascular System > Cellular and Molecular Events in the CVS > Flashcards

Cellular and Molecular Events in the CVS Flashcards

1
Q

Does Na/K-ATPase set the RMP?

A

No

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2
Q

What happens to RMP if the sodium pump is blocked?

A

It only changes by 5-7mV

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3
Q

What is the RMP set by?

A

Due to K permeability of the cell membrane at rest

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4
Q

What state are K channels in at rest?

A

Open

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5
Q

What channels do cardiac myocytes possess?

A

Inward rectifier K channels

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6
Q

How permeable to other ions are cardiac myocytes?

A

Only a small permeability

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7
Q

What can be said of cardiac myocytes?

A

They are electrically active

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8
Q

What is meant by cardiac myocytes being electrically active?

A

They fire action potentials

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9
Q

What do action potentials trigger?

A

An increase in cytosolic [Ca]

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10
Q

What is a rise in calcium required for?

A

To allow actin and myosin interaction

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11
Q

What does actin and myosin interaction generate?

A

Tension (contraction)

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12
Q

How do action potentials in heart cells differ from those in nerves and skeletal muscle?

A

They are much longer

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13
Q

What are the stages in the ventricular (cardiac) action potential?

A

Opening of voltage gated Na channels causes a rapid depolarisation, from RMP to +30mV as Na enters the cell
Transient outward K current causes a return towards a lower membrane potential, reaching +10mV
Membrane potential lowers to about -10mV because of opening of voltage gated Ca channels
Ca channels inactivate and voltage gated K channels open, causing return to RMP

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14
Q

What is rapid depolarisation due to opening of Na channels called?

A

The upstroke

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15
Q

What might happen after the initial depolarisation that contributes to a lower membrane potential?

A

Might get some reversal of Na/Ca transport

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16
Q

What may also happen when the voltage gated Ca channels are open?

A

May be some K channels open, allowing efflux of K

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17
Q

What do cardiac myocytes possess lots of different types of?

A

K channels

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18
Q

Draw the ventricular action potential

A

Answer…

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19
Q

Why do cardiac myocytes have lots of different types of K channels?

A

Because they each behave in a different way, and contribute differently to the electrical properties of the cell

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20
Q

What is the SA nodes set membrane potential?

A

Doesn’t really have one

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21
Q

Why does the SA node not really have a set membrane potential?

A

Because the whole time, there is a long, slow depolarisation

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22
Q

What is the SA nodes long, slow depolarisation called?

A

The pacemaker potential

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23
Q

What causes the pacemaker potential?

A

Influx of Na

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24
Q

What happens as Na channels open?

A

Na ions go in to cause a little bit of depolarisation, but become inactivated in accommodation due to long depolarisation

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25
Q

What is the result of the Na channels becoming inactivated by the long depolarisation?

A

The upstroke cannot rely on Na channels, it also needs voltage gated Ca channels

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26
Q

What is the initial slope to threshold of the SA node action potential known as?

A

The funny current

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27
Q

When is the SA node action potential activated?

A

When it reaches membrane potentials that are more negative than -50mV

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28
Q

What is the result on the SA node action potential when the membrane potential reaches a more negative level?

A

The more it activates

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29
Q

What channels does the funny current use?

A

HCN

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30
Q

How are HCN channels activated?

A

Hyperpolarisation

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31
Q

How are HCN channels controlled?

A

Cyclic nucleotide-gated

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32
Q

What do HCN channels allow?

A

Influx of Na ions, which depolarises the cell

33
Q

Describe the process of the SA node action potential

A

Voltage gated Ca channels when the membrane potential reaches -50mV, causing depolarisation
Opening of voltage gated K channels cause repolarisation

34
Q

What does the opening of voltage gated Ca channels cause in the SA node action potential?

A

Upstroke

35
Q

What does the opening of voltage gated K channels cause in the SA node action potential?

A

Downstroke

36
Q

How does the SA node action potential differ from the ventricular?

A

It is not as quick

37
Q

Why is the SA node action potential not as quick as the ventricular?

A

Because calcium channels open more slowly

38
Q

What is the SA node action potential said to have?

A

Natural automaticity

39
Q

What is said of the membrane potential of the SA node?

A

It is unstable

40
Q

Does the action potential waveform stay the same throughout the heart?

A

No, it varies

41
Q

What part of the heart is fastest to depolarise?

A

SA node

42
Q

What is the result of the SA node being the fastest to depolarise?

A

It sets the rhythm

43
Q

What other parts of the conduction system have automaticity?

A

AV node

44
Q

Why doesn’t the AV node set the rhythm?

A

It depolarises slower

45
Q

What path does the cardiac action potential take?

A

Travels from SA node, to AV node, down bundle of His to bundle branches

46
Q

What are the bundle branches in the heart?

A

Left (posterior division)
Left (anterior division)
Right

47
Q

What are the features of cardiac muscle?

A

Striated
Branching pattern
Intercalated discs
Single central nuclei

48
Q

How are cardiac muscle cells joined?

A

Structurally by desmosomes

Electrically by gap junctions

49
Q

What do desmosomes do?

A

Rivet cells together

50
Q

What do gap junctions do?

A

Allow for rapid transfer of ions

51
Q

What does depolarisation that happens during the ventricular action potential do?

A

Opens L-type Ca channels in the T-tubule system

52
Q

Where is the T-tubule system localised?

A

Close to the SR

53
Q

What does localised Ca entry due to channels opening cause?

A

Opening of calcium-induced calcium release (CICR) channels in the sarcoplasmic reticulum

54
Q

What is closely linked to L-type channels?

A

Ca release channels

55
Q

What % of calcium enters across the sacrolemma, through L type channels?

A

25%

56
Q

What % of calcium is released from the SR?

A

75%

57
Q

How is cardiac myocyte contraction regulated?

A

Ca binds to troponin C, and a conformational change shifts tropomyosin to reveal myosin binding site on actin filament

58
Q

What must happen to relax cardiac myocytes?

A

Must return intracellular [Ca] to normal levels

59
Q

How is intracellular [Ca] returned to normal levels?

A

Most pumped back into SR

Some exits across plasma membrane

60
Q

How is Ca pumped back into the SR?

A

SERCA

61
Q

What stimulates the SERCA pumps?

A

Raised [Ca]

62
Q

How does Ca exit across the cell membrane?

A

Sarcolemmal Ca-ATPase

Na/Ca exchanger

63
Q

What is tone of blood vessels controlled by?

A

Contraction and relaxation of vascular smooth muscle cells

64
Q

Where are the vascular smooth muscle cells located?

A

In the tunica media

65
Q

What is present in the tunica media?

A

Multiple circularly arranged smooth muscle layers

66
Q

What vessels have vascular smooth muscle cells?

A

Arteries, arterioles and veins

67
Q

How is vascular smooth muscle different from striated muscle?

A

Don’t have the same arrangement of actin and myosin

68
Q

How are actin and myosin arranged in vascular smooth muscle?

A

Connected to dense bodies, and radiate out

69
Q

At what level does regulation of cardiac contraction occur?

A

Of the myosin head

70
Q

How does the myosin head regulate cardiac contraction?

A

It has a regulatory light chain

71
Q

What happens when light chain on the myosin head is not phosphorylated?

A

It can’t bind to actin

72
Q

How is myosin activated?

A

Myosin light chain kinase (MLCK) phoshorylates myosin

73
Q

Why does MLCK need to be controlled itself?

A

To prevent it from activating myosin all the time, and contraction happening all the time

74
Q

How is MLCK controlled?

A

Calmodulin

75
Q

How does calmodulin activate MLCK

A

Calmodulin can bind 4 calcium ions. Calcium can either
come from voltage gated calcium channels, or from SR.

In smooth muscle cells, there are adrenoreceptors- α-1
receptors. If noradrenaline binds these receptors, it causes production of IP 3
which then causes release of calcium from SR. Calcium binds to
calmodulin, which activates MLCK.

76
Q

How is MLCK activation terminated?

A

Myosin light chain phosphatases

77
Q

When are MLCPs active?

A

Constitutively- active all the time

78
Q

How are MLCPs regulated?

A

When noradrenaline binds to alpha-1 receptor, also
forms DAG, which activates protein kinase C- phosphorylates MLCP, inhibiting
it.

79
Q

Why is there relaxation as Ca levels decline?

A

As myosin light chain
phosphatase dephosphorylates the myosin light chain (no longer inhibited as
noradrenaline not binding)

ESA 2- Cardiovascular System (18 decks)

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