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CVS > Electrical And Molecular Mechanisms Of The Heart And Vasculature > Flashcards

Electrical And Molecular Mechanisms Of The Heart And Vasculature Flashcards

1
Q

What is the most important factor about a cardiac myocyte which makes it polarised at rest?

A

Permeability to K+ ions at rest

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2
Q

Which direction do K+ move when the cardiac myocyte is at rest?

A

From inside to outside the cell (down the concentration gradient)

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3
Q

At rest, what is the relative membrane potential across a cardiac myocyte?

A

Negative inside the cell, positive outside the cell

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4
Q

What other ion transporter has a small contribution to maintaining resting membrane potential and how does it do this?

A

Na+/K+ ATPase

Pumps 3 Na+ out against its concentration gradient and 2K+ in.
This contributes to making the outside of the membrane more electro positive than the inside contributing to the ELECTROCHEMICAL gradient

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5
Q

At what point does the net-outflow of K+ in cardiac myocytes at rest cease and what is this called?

A

When concentration of K+ outside = inside

Equilibrium potential for K+ (Ek)

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6
Q

Why is resting membrane potential (RMP) not equal to the equilibrium potential for K+ (Ek) when the main determinant for RMP is permeability to K+ at rest?

A

Cardiac myocytes have very small permeability to other ions at rest

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7
Q

What is an action potential?

A

Rapid sequence of changes in membrane potential across a membrane

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8
Q

What structures between cardiac myocytes make them electrically coupled?

A

Intercalated discs/gap junctions

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9
Q

The influx of what ion into the cell following an action potential ultimately leads to muscle contraction?

A

Ca2+

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10
Q

Relatively compare the duration of an action potential of skeletal muscle to a cardiac ventricle:

A

Skeletal muscle = short
Cardiac ventricle = long

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11
Q

What is the rough resting membrane potential of a cardiac myocyte?

A

-80mV to -90mV

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12
Q

What is the rough Ek of a cardiac myocyte?

A

-95mV

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13
Q

What are the 4 general events that occur in a cardiac myocyte action potential?

A

UPSTROKE
INITIAL REPOLARISATION
PLATEAU
REPOLARISATION

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14
Q

The opening of what channels and influx of what ion causes the rapid depolarisation (UPSTROKE) in an action potential?

A

Voltage gated Na+ channels open

Rapid influx of Na+

Makes inside of cell more POSITIVE

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15
Q

What causes the initial repolarisation stage in an action potential?

A

Transient/short-lived outward K+ current
(Makes cell more negative)

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16
Q

What occurs at the plateau (Very gradual repolarisation) stage of a cardiac action potential?

A

Voltage gated Ca2+ channels open (Ca2+ INFLUX)

Some K+ channels open allowing K+ EFFLUX (why cell doesn’t rapidly depolarise/get more positive quickly)

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17
Q

What happens in the repolarisation stage of the cardiac action potential?

What ion is mainly being moved?

A

Voltage gated Ca2+ channels inactivate/close

Voltage gated K+ channels open

RAPID K+ EFFLUX

Cardiac myocyte returns to resting membrane potential (-80mV to -90mV)

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18
Q

If a ventricular action potential was described in terms of influx and efflux of ions, describe the stages:

A

RMP
Upstroke/depolarisation = Na+ INFLUX
Initial repolarisation = Transient K+ EFFLUX
Plateau = Ca2+ INFLUX Some K+ efflux
Repolarisation = EFFLUX of K+ Ca2+ channels close

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19
Q

Where are pacemaker cells located in the heart?

A

Sino-atrial node (SAN)
Atrio-ventricular Node (AVN))

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20
Q

What is special about pacemaker cells?

A

Can spontaneously depolarise and fire action potentials

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21
Q

Why can pacemaker cells spontaneously depolarise?

A

Have a different mix of ion channels to normal cardiac myocytes

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22
Q

What feature of the SAN cells enables them to be the pacemakers of the cell?

A

Fastest cells to depolarise

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23
Q

Roughly what is the lowest the membrane potential reaches in a SAN cell (pacemaker) and what does this mean?

A

About -60mV

Never truly at rest

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24
Q

Briefly describe how the steps of an action potential in the SAN:

A

Very gradual increase in membrane potential (slow depolarisation) from -60mV to -50mV
At -50mV activated and rapid depolarisation
Then rapid repolarisation to -60mV
Repeat

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25
Q

What is the threshold potential for SAN cells?

A

-50mV

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26
Q

What is the name of the gradual slope/slow influx of Na+ that causes threshold potential to be reached in a SAN (pacemaker) cell?

A

Funny current (If) I little f

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27
Q

What causes the rapid depolarisation (UPSTROKE) once threshold has been reached in a pacemaker cell and how does this differ to a ventricular cardiac myocyte?

A

Voltage gated Ca2+ channels open = RAPID Ca2+ INFLUX

Depolarisation caused by rapid influx of Na+ once voltage gated Na+ channels open in ventricular cardiac myocyte not CA2+

28
Q

What causes the rapid repolarisation back to -60mV in a pacemaker cell

A

Voltage gated K+ channels open

Rapid K+ EFFLUX

29
Q

When the cell is hyperpolarised, which channel allows the gradual influx of Na+ causing the funny current? (SAN)

A

HCN channel

30
Q

What is the role of the Sino-atrial node?

A

Sets the rhythm of the cell (pacemaker) since its the fastest to depolarise

31
Q

If the Sino-atrial cells stopped working and producing action potentials, which part of the heart would take over as the pacemaker and why?

A

Atrioventricular node
The second fastest part to depolarise

32
Q

What is the name of the condition if action potentials fire too slowly in the heart?

A

Bradycardia

33
Q

What happens if action potentials fire too quickly in the heart ?

A

Tachycardia

34
Q

What happens if electrical activity of the heart becomes random?

A

Fibrillation

35
Q

What is it called when action potentials in the heart fail (no electrical activity)?

A

Asystole

36
Q

What is the normal range for plasma potassium [K+]?

A

3.5mmol/L - 5.5mmol/L

37
Q

What is it called when plasma [K+] is below 3.5mmol/L?

A

Hypokalaemia

38
Q

What is it called when plasma [K+] exceeds 5.5mmol/L?

A

Hyperkalaemia

38
Q

What is it called when plasma [K+] exceeds 5.5mmol/L?

A

Hyperkalaemia

39
Q

Why are cardiac myocytes so sensitive to changes in [K+]?

A

K+ permeability main contributor to RMP

40
Q

How does hyperkalaemia affect the action potentials in a cardiac myocyte?

A

RMP is more depolarised (more positive)
This inactivates some Voltage gated Na+ channels causing slower upstroke

41
Q

With hyperkalaemia, how is the Ek value affected of the cardiac myocyte?

A

Ek = more positive/less negative

More K+ on outside, less K+ needs to move out to reach equilibrium

42
Q

How can severe hyperkalaemia cause asystole?

A

Causes RMP to be very positive (myocytes very depolarised all the time)

Voltage gated Na+ channels always inactivated so NO UPSTROKE

43
Q

How can hyperkalaemia be treated?

A

Calcium gluconate (acts a shield reduces excitability)

Insulin + Glucose (Ins promotes cellular uptake of K+ reducing plasma [K+] and glucose prevents hypoglycaemia from insulin intake)

44
Q

What is the effect of Hypokalaemia on cardiac myocyte action potentials?

A

Lengthens action potential delaying repolarisation

45
Q

How does hypokalaemia lengthen the action potential/delay repolarisation?

A

Reduces conductance of K+ channels slowing K+ efflux

46
Q

What is the problem that longer depolarisations due to hypokalaemia can cause?

A

Early after depolarisations (EADs)
Oscillations in membrane potentials
Ventricular fibrillation (type of arrhythmia)

47
Q

Briefly describe how an action potential causes a contraction in a cardiac myocyte:

A

Action potential travels deep through T-tubules and across surface of myocyte (influx of Na+)
Voltage gated Ca2+ channels on plasma membrane open (Ca2+ INFLUX)
Voltage gated Ca2+ channels on Sarcoplasmic Reticulum (SR) release lots of Ca2+ into cytoplasm (Calcium Induced Calcium Release)
Ca2+ interacts with muscle filaments and contraction occurs

48
Q

How does Ca2+ in the cytoplasm of the cardiac myocyte induce contraction?

A

Ca2+ binds to Troponin C on Tropomyosin complex which shields actin from myosin
Causes conformational change of Tropomyosin revealing binding site for mysosin head on actin
Actin-myosin cross bridges form and power stroke occurs

49
Q

What occurs during cardiac myocyte relaxation, after an action potential?

A

[Ca2+] returned to resting levels

50
Q

How is [Ca2+] returned back to resting levels during cardiac myocyte relaxation?

A

SERCA (SarcoEndoplasmic reticulum Ca2+ ATPase) pumps Ca2+ back into SR
NCX (Na+ Ca2+ exchanger) pumps Ca2+ out of sarcolemma

51
Q

What type of muscle cells are present in the tunica media layers of blood vessels?

A

Smooth muscle

52
Q

Which blood vessels is vascular smooth muscle found in?

A

Arteries
Arterioles
Veins

53
Q

What does MLCK stand for?

A

Myosin Like Chain Kinase

54
Q

What does MLCP stand for?

A

Myosin Like Chain Phosphatase

55
Q

Where is MLCK and MLCP found in the body?

A

Smooth muscle cells

56
Q

Why are MLCK and MLCP needed in smooth muscle? What regulating complex is not present in smooth muscle that is present in cardiac muscle?

A

Smooth muscle = no troponin

57
Q

What 2 structures on the plasma membrane of a smooth muscle cell are important in initiating muscle contraction? (A channel and a receptor)

A

Voltage gated Ca2+ channels
Alpha adrenoceptors

58
Q

What is the role of MLCK in smooth muscle contraction?

A

It Phosphorylates the myosin head activating it

59
Q

What is the role of MLCP in smooth muscle contraction?

A

Dephosphorylates myosin head deactivating it allowing muscle to relax

60
Q

What molecule activates MLCK?

A

Ca2+ Calmodulin complex

61
Q

How many Ca2+ molecules bind to Calmodulin so that it can activate MLCK?

A

4

62
Q

What are the 2 methods by which Calmodulin becomes saturated with Ca2+ so that it can bind to and activated MLCK?

A

Ca2+ influx via Voltage gated Ca2+ channels

Noradrenaline binds to alpha adrenoceptors leading to production of secondary messenger which stimulates SR to release Ca2+ into cytoplasm

63
Q

Does the Myosin light chain on the myosin head need to phosphorylated or dephosphorylated for actin-myosin interaction to occur?

A

Phosphorylated

64
Q

How does noradrenaline stimulate smooth muscle contraction?

A

Binds to A1 adrenoceptors, activates the Gq protein subunits producing IP3 and DAG, IP3 binds to receptoron sarcoplasmic endoplasmic reticulum stimulating Ca2+ release and DAG activates PKC (protein kinase C) which inactivates MLCP

Stimulates SR to release Ca2+ saturating Calmodulin so MLCK can phosphorylate the light chain

Also inhibits MLCP activity so muscle stays contracted

65
Q

Can MLCK be phosphorylated and what is its relevance?

A

Yes
Important for autonomic nervous system

CVS (21 decks)

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