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CVS > 4. Electrical Control > Flashcards

4. Electrical Control Flashcards

1
Q

Is the conc K+ higher or lower inside cardiac myocytes than extracellularly?

A

Higher inside

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2
Q

Is the concentration of Na+ higher or lower inside cardiac myocytes than extracellularly?

A

Lower inside

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3
Q

What sets up the resting membrane potential in cardiac myocytes?

A

Permeable to K+, so moved out of cell, making inside negative. There is very small permeability to other ion species, making the RMP not quite equal to Ek.

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4
Q

What is the resting membrane potential of cardiac myocytes?

A

-90 to -85 mV

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5
Q

What does an action potential in cardiac myocytes trigger an increase in for contraction?

A

Cytosolic Ca2+ conc

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6
Q

What causes the upstroke in the ventricular action potential?

A

Opening of voltage gated Na+ channels causing an influx of Na+

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7
Q

What causes the initial repolarisation in the cardiac action potential?

A

Opening of voltage-gated K+ channels and so an transient outward movement of K+

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8
Q

What causes the plateau in the cardiac action potential around 0mV?

A

Opening of voltage-gated Ca2+ channels and so influx of Ca2+ which balances with the K+ efflux

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9
Q

What causes repolarisation in the cardiac action potential?

A

Ca2+ channels inactivate and voltage-gated K+ channels remain open, so K+ efflux, making inside cell more negative again

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10
Q

Do the cells in the sinoatrial node have a resting membrane potential?

A

No, as they spontaneously depolarise

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11
Q

In the sinoatrial node, what is the name of the initial slope to threshold? What causes it?

A

Funny current

HCN channels - Na+ channels, influx of Na+ depolarises the cell

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12
Q

What causes the upstroke in the sinoatrial node action potential?

A

Opening of voltage-gated Ca2+ channels and Ca2+ influx

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13
Q

What causes sinoatrial node repolarisation?

A

Closing of Ca2+ channels and opening of voltage-gated K+ channels and K+ efflux

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14
Q

What type of voltage-gated Ca2+ channels are involved in cardiac myocytes and SA action potentials?

A

L-type

Then CICR in the SR

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15
Q

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

A

Bradycardia

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16
Q

What happens if the action potentials in the heart fail?

A

Asystole (heart ceases to beat)

17
Q

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

A

Tachycardia

18
Q

What happens if the electrical activity in the heart becomes random?

A

Fibrillation

19
Q

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

A

RMP is so close to Ek and K+ permeability dominates the resting membrane potential

20
Q

What effect does hyperkalaemia (high blood plasma K+ levels) have on cardiac myocytes?

A

Depolarises the myocytes as Ek gets less negative

Slows upstroke of action potential by inactivating some voltage-gated Na+ channels

21
Q

What is the main risk with hyperkalaemia?

A

Asystole

22
Q

What is the treatment for hyperkalaemia?

A

Calcium gluconate - makes heart less excitable
Insulin + glucose - promotes K+ movement into cells
NB dont work if heart has already stopped beating

23
Q

What affect does hypokalaemia (low plasma K+ conc) have on the action potential of cardiac myocytes?

A

Lengths the action potential
Delays repolarisation
Longer action potentials lead to early after depolarisations, and oscillations in membrane potential

24
Q

What is the main risk with hypokalaemia?

A

VF and tachycardia

25
Q

How does Ca2+ cause cardiac myocytes contraction?

A

Ca2+ binds to troponin C
Conformational change moves tropomyosin, to reveal myosin binding site on actin filament. Myosin head then binds to myosin binding site on actin

26
Q

How does Ca2+ conc return to resting levels in repolarisation?

A

SERCA - pumps back into SR

Sarcolemmal Ca2+ ATPase and Na+/Ca2+ exchanger - Ca2+ exits across cell membrane

27
Q

Where are the vascular smooth muscle cells located in blood vessels?

A

Tunica media

28
Q

What are the two ways of increasing Ca2+ conc in excitation contraction coupling in vascular smooth muscle?

A

Depolarisation opening voltage gated calcium channels

Noradrenaline activating the alpha1 receptors

29
Q

What does calcium bind to in excitation contraction coupling in vascular smooth muscle? What does it activate?

A

Calmodulin

MLCK

30
Q

What needs phosphorylating in excitation contraction coupling in vascular smooth muscle to permit action with actin?

A

Myosin LIGHT chain

31
Q

What inhibits the action of MLCK in excitation contraction coupling in vascular smooth muscle?

A

Phosphorylation of MLCK by PKA

CVS (14 decks)

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