Pacemaker cells

Question 1

What determines the resting membrane potential

Answer 1

The permeability of the membrane to different ions

Question 2

What distributes Na+ and K+, what drives this?

Answer 2

Na+-K+ ATPase; 3 Na+ out, 2K+ in

*keeps electrochemical (-ve) and concentration gradients

Question 3

What are the resting membrane potentials for the following ions…K+Na+Cl-

Answer 3

Cl-/K+ is -90 mV: if you let all K+ out, RMP would become -90 mV

Na+ higher outside cell: +50 mV

Question 4

What determines the equilibrium?

Answer 4

Balance of concentration and electrochemical charge gradient

Question 5

Briefly describe the myocardial AP

What happens in depolarization of cardiac cells?

Answer 5

1. Rapid upstroke: Na+ channels open -> RMP more +ve
2. Initial repolarization: VGNa+ inactivated, K+ opens
3. Calcium channels open, balanced K+ loss and keeps membrane potential +ve -> stimulates SER to release calcium stores *calcium channels stay open 250 ms (time of systole)
4. Rapid repolarization: Ca2+ channels close, more K+ open -> MP comes back to -90mV

Question 6

What shape is the pacemaker’s AP, where does this occur?

why is it different than a normal cardiac cell’s?

Answer 6

SA and AV nodes: Short and triangular NO fast sodium channels (only HCN channels)

1. Upstroke: slow opening Ca2+ channels
2. Repolarization: closes Ca2+ channels, opens K+ = gradual downward

Question 7

What stops hyperpolarisation in pacemaker cells from never-ending?

Answer 7

HCN channels/funny current -> allows Na+ in so RMP reaches threshold for Ca2+ channels to reopen

Question 8

How does sympathetic/parasympathetic innervation affect the depolarization of pacemaker cells?

Answer 8

Sympathetic: NA steepens slope, next AP generated faster

Parasympathetic: Ach shallows slope, HR lowers

Question 9

How does the myocardial AP differ from skeletal muscle? (3)

Answer 9

1. has a plateau due to Ca2+ influx and K+ efflux
2. contraction requires CICR
3. cardiac myocytes electrically coupled via gap junctions