Cellular and Molecular Events in the CVS Flashcards Preview

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

Flashcards in Cellular and Molecular Events in the CVS Deck (79):
1

Does Na/K-ATPase set the RMP?

No

2

What happens to RMP if the sodium pump is blocked?

It only changes by 5-7mV

3

What is the RMP set by?

Due to K permeability of the cell membrane at rest

4

What state are K channels in at rest?

Open

5

What channels do cardiac myocytes possess?

Inward rectifier K channels

6

How permeable to other ions are cardiac myocytes?

Only a small permeability

7

What can be said of cardiac myocytes?

They are electrically active

8

What is meant by cardiac myocytes being electrically active?

They fire action potentials

9

What do action potentials trigger?

An increase in cytosolic [Ca]

10

What is a rise in calcium required for?

To allow actin and myosin interaction

11

What does actin and myosin interaction generate?

Tension (contraction)

12

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

They are much longer

13

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

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

14

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

The upstroke

15

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

Might get some reversal of Na/Ca transport

16

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

May be some K channels open, allowing efflux of K

17

What do cardiac myocytes possess lots of different types of?

K channels

18

Draw the ventricular action potential

Answer…

19

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

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

20

What is the SA nodes set membrane potential?

Doesn’t really have one

21

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

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

22

What is the SA nodes long, slow depolarisation called?

The pacemaker potential

23

What causes the pacemaker potential?

Influx of Na

24

What happens as Na channels open?

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

25

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

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

26

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

The funny current

27

When is the SA node action potential activated?

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

28

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

The more it activates

29

What channels does the funny current use?

HCN

30

How are HCN channels activated?

Hyperpolarisation

31

How are HCN channels controlled?

Cyclic nucleotide-gated

32

What do HCN channels allow?

Influx of Na ions, which depolarises the cell

33

Describe the process of the SA node action potential

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

34

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

Upstroke

35

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

Downstroke

36

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

It is not as quick

37

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

Because calcium channels open more slowly

38

What is the SA node action potential said to have?

Natural automaticity

39

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

It is unstable

40

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

No, it varies

41

What part of the heart is fastest to depolarise?

SA node

42

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

It sets the rhythm

43

What other parts of the conduction system have automaticity?

AV node

44

Why doesn’t the AV node set the rhythm?

It depolarises slower

45

What path does the cardiac action potential take?

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

46

What are the bundle branches in the heart?

Left (posterior division)
Left (anterior division)
Right

47

What are the features of cardiac muscle?

Striated 
Branching pattern 
Intercalated discs 
Single central nuclei

48

How are cardiac muscle cells joined?

Structurally by desmosomes 
Electrically by gap junctions

49

What do desmosomes do?

Rivet cells together

50

What do gap junctions do?

Allow for rapid transfer of ions

51

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

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

52

Where is the T-tubule system localised?

Close to the SR

53

What does localised Ca entry due to channels opening cause?

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

54

What is closely linked to L-type channels?

Ca release channels

55

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

25%

56

What % of calcium is released from the SR?

75%

57

How is cardiac myocyte contraction regulated?

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

58

What must happen to relax cardiac myocytes?

Must return intracellular [Ca] to normal levels

59

How is intracellular [Ca] returned to normal levels?

Most pumped back into SR
Some exits across plasma membrane

60

How is Ca pumped back into the SR?

SERCA

61

What stimulates the SERCA pumps?

Raised [Ca]

62

How does Ca exit across the cell membrane?

Sarcolemmal Ca-ATPase
Na/Ca exchanger

63

What is tone of blood vessels controlled by?

Contraction and relaxation of vascular smooth muscle cells

64

Where are the vascular smooth muscle cells located?

In the tunica media

65

What is present in the tunica media?

Multiple circularly arranged smooth muscle layers

66

What vessels have vascular smooth muscle cells?

Arteries, arterioles and veins

67

How is vascular smooth muscle different from striated muscle?

Don’t have the same arrangement of actin and myosin

68

How are actin and myosin arranged in vascular smooth muscle?

Connected to dense bodies, and radiate out

69

At what level does regulation of cardiac contraction occur?

Of the myosin head

70

How does the myosin head regulate cardiac contraction?

It has a regulatory light chain

71

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

It can’t bind to actin

72

How is myosin activated?

Myosin light chain kinase (MLCK) phoshorylates myosin

73

Why does MLCK need to be controlled itself?

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

74

How is MLCK controlled?

Calmodulin

75

How does calmodulin activate MLCK

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

How is MLCK activation terminated?

Myosin light chain phosphatases

77

When are MLCPs active?

Constitutively- active all the time

78

How are MLCPs regulated?

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

79

Why is there relaxation as Ca levels decline?

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