Electrical and molecular mechanisms in the heart

Question 1

What determines the resting membrane potential?

Answer 1

The permeability of the membrane to K+

Question 2

Why isn’t the resting membrane potential the same as the equilibrium potential of K+?

Answer 2

The membrane is permeable to other ions eg. Na+

Question 3

What are the maximum and minimum values of the membrane potential in ventricular myocyte action potential?

Answer 3

-70 to +30

Question 4

How long does 1 action potential last? How long is the plateau in the action potential? Releative to the systole, how long does diastole last for?

Answer 4

300ms
200ms
twice as long as systole

Question 5

Describe the four stages of the ventricular myocyte action potential

Answer 5

1. VG Na+ channels open, so Na+ enters the cell, so depolarisation
2. Na+ channels inactivate as depolarised. VG K+ channels open so temporary decrease in membrane potential
3. VG Ca2+ channels open. Ca2+ enters the cell, so plateau
4. VG Ca2+ channels inactivate. VG K+ channels open, so K+ efflux–>repolarisation of the cell

Question 6

What are the axes labelled with in the ventricular and SAnode action potential graphs?

Answer 6

membrane potential (Y)
time (X)

Question 7

Describe the three steps in the Staphylococcus Aureus node action potential

Answer 7

1. Funny vurrent. Na+ enters via HCN channels–>shallow depolarisation
2. When the cell reaches threshold potential, VG Ca2+ channels open–>depolarisation
3. K+ channels open leading to repolarisation

Question 8

What is the range of the membrane potential of the Staphylococcus Aureus node?

Answer 8

-60 to +30

Question 9

What is the effects of hyperpolarisation on the HCN channels?

Answer 9

Hyperpolarisation–>more HCn channels opening, so incrwaded influx of Na+

Question 10

What is the effect of hyperkalaemia on the Ventricular action potential

Answer 10

increased K+–>less -ve membrane potential–>more inactivation of Na+ channels, so slower uptake of Na+ so slower depolarisation of membrane, upstroke slower

Question 11

effect of hyperkalaemia on the SAnode action potential

Answer 11

less negative membrane potential,so less HCN are activated, so less Na+ enters the cell, so slower uptake of Na+–>longer time to reach the threshold potential
so bradycardia

Question 12

what is the danger of hyperkalaemia?

Answer 12

asystole

Question 13

what is the effect on the vent AP of hypokalaemia?

Answer 13

longer downstroke. Risk of arrythmias

Question 14

Describe the contraction mechanism of cardiac myocytes

Answer 14

depolarisation–>opening of VG Ca2+ channels–>Ca2+ influx
Ryanodine receptors open via CICR –> Ca2+ efflux from the SER
Ca2+ binds to troponin, moving tropomyosin out of the way so myosin heads can bind to actin filaments

Question 15

What happens at the end of the contraction in cardiac myocytes?

Answer 15

Ca2+ pumped back into SER by SERCA and some Ca2+ crosses the membrane via Ca2+ ATPase and Na+/Ca2+ exchanger

Question 16

Describe the mechanism of smooth muscle contraction

Answer 16

depolarisation across the cell
VGCa2+ channels open
Ca2+ enters the cell

also noradrenaline binds to a GPCR that cleaves G alpha Q that causes the cleaving of PIP2 into IP3 and DAG
IP3 binds to IP3R allowing Ca2+ to rush out of the SER

Ca2+ binds to calmodulin. the calcium calmodulin complex activates MLCK
MLCK phospharylates myosin light chain, activating it so it can bind to actin filaments

Question 17

describe the regulation of smooth muscle cell contraction (2 ways)

Answer 17

protein kinase A can phosphorylate MLCK and inhibit its action
also MLC phosphatase can dephosphorylate Myosin regulatory light chain
MLC phosphatase itself can be phosphorylated by PKC which is activated by DAG. Protein Kinase C reduces the activty of MLC phosphatase so increases contraction