Electrical And Molecular Mechamisms

Question 1

Describe how resting membrane potential of cardiac cells is generated

Answer 1

Potassium permeability sets the resting potential
Cardiac myocytes are permeable to potassium at rest
Small movement of ions makes the inside negative with respect to outside
Resting potential set at -90mV to -85mV

Question 2

Are SA node and ventricular action potentials longer or shorter than axon action potentials

Answer 2

Longer

Question 3

Draw the ventricular (cardiac) action potential

Answer 3

See onenote

Question 4

Describe the stages of ventricular action potential

Answer 4

1. Upstroke occurs where sodium channels open with depolarisation and then inactivate
2. Initial repolarisation due to transient outward potassium current
3. Plateau phase due to opening of L-type voltage gated calcium channels whilst some potassium channels also open - allows all myocytes in myocardium to begin action potential
4. Calcium channels inactivate and more voltage gated potassium channels open

Question 5

Draw the sino-atrial action potential

Answer 5

See onenote

Question 6

Describe the stages of sino-atrial node action potential

Answer 6

1. Pacemaker potential - slow depolarisation to threshold (funny current - If)
   Influx of sodium and some potassium until -50mV threshold
2. At threshold, upstroke due to L-type voltage gated calcium channel open
3. Repolarisation due to opening of voltage gated potassium channels lowers potential to -60mV

Question 7

Describe the process of excitation-contraction coupling in ventricular myocardial cells

Answer 7

SA node is fastest to depolarise - sets rhythm (pacemaker)
Big gap junctions in myocytes allow quick transmission of electrical signals
Action potential opens L-type calcium channels in T-tubule system
Calcium inside calcium release triggers release of calcium from SR through ryanodine receptor
L-type calcium channels and ryanodine receptor closely linked

Question 8

How is cardiac myocyte contraction regulated

Answer 8

Calmodulin levels control amount of phosphorylation of myosin heads
Relaxation as calcium levels decline
Phosphorylation of MLCK by PKA inhibits action of MLCK

Question 9

Explain the detailed release of calcium causing contraction

Answer 9

1. Alpha-1 receptors linked to Gq subunit stimulates production of IP3 causing release of calcium in SR
2. Activates calmodulin binds to myosin light chain kinase (MLCK), causing phosphorylation of light chain on myosin head using ATP
3. Allows binding to action and contraction to take place
4. Myosin light chain phosphatase (MLCP) enzyme dephosphorylates light chain

Question 10

What is normal plasma potassium concentration

Answer 10

3.5 - 5.5 mmol/L

Question 11

Why is it important for myocytes to have a normal plasma potassium concentraiton

Answer 11

Myocytes very sensitive to changes in potassium concentration as potassium ions set resting potential

Question 12

What are the effects of hyperkalaemia

Answer 12

By increasing potential concentration outside, Ek becomes less negative so membrane depolarises slightly (higher resting potential)
Inactivate some sodium channels meaning they are unavailable for upstroke of action potential
Slower upstroke
May initially get an increase in excitability

Question 13

How can you treat hyperkalaemia

Answer 13

Calcium gluconate - makes heart less excitable by increasing threshold potential
Insulin and glucose promotes potassium entering cells to lower serum potassium levels

Question 14

What are the effects of hypokalaemia

Answer 14

Lengthens the action potential and delays repolarisation
Lead to early depolarisation causing oscillations in membrane potential
Can result in ventricular fibrillation