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A Physiology > 2.1A. Impulse generation and conduction in the heart. Mechanism of pacemaker potential. Control of pacemaker activity and impulse conduction. > Flashcards

2.1A. Impulse generation and conduction in the heart. Mechanism of pacemaker potential. Control of pacemaker activity and impulse conduction. Flashcards

1
Q

I. Impulse generation in the heart
1/ What type of cells does the heart consist of?

A

Contractile cells and conducting cells

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2
Q

I. Impulse generation in the heart
2/ What is the role of conducting cells?

A
  • Primarily responsible for impulse generation and pacemaker activity found in SA node in right atrium
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3
Q

I. Impulse generation in the heart
3/ What are the 2 main types of AP?

A
  • Fast response AP
  • Low-response AP
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4
Q

I. Impulse generation in the heart
4/ What are the 5 phases of AP?

A

Phase…
0: upstroke
1: partial repolarization
2: plateau
3: complete repolarization
4: resting membrane potential

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5
Q

I. Impulse generation in the heart
5/ Where does low-response AP occur?

A

In nodal cells

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6
Q

I. Impulse generation in the heart
6/ What are the differences between the fast and slow-response AP? What can you conclude about slow-response AP?

A

1/ Resting membrane potential (phase 4) is more negative in fast-response AP
2/ Slow-response AP does not have phase 1 and 2
3/ Slope of upstroke phase of AP is greater in fast-response AP
4/ Amplitude of AP is greater in fast-response AP
=> AP (conduction) is propagated more slowly and more likely to be blocked in the slow-response nodal tissues compared to fast-response myocardium

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7
Q

II. Mechanism of pacemaker potential
1/ What is the property of pacemaker cells (SA node)?

A

It has the property of automaticity, meaning it spontaneously depolarizes and generate AP

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8
Q

II. Mechanism of pacemaker potential
2/ What are the key ions in AP generation?

A

Na+, Ca2+, K+

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9
Q

II. Mechanism of pacemaker potential
3/ What are the 5 ion channels participate in the development of pacemaker potential?

A

1/ HCN (hyper-polarization activated cyclic nucleotide gated-cation channel)
2/ T-type VD Ca2+ channels
3/ L-type VD Ca2+ channels
4/ VD K+ channels
5/ GIRKs (G-protein coupled inwardly rectified K+ channels)

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10
Q

II. Mechanism of pacemaker potential
4/ What are the characteristics of HCN?

A
  • Non-selective cation channel
  • Activated by hyper polarization to around -50 mV
  • An influx of Na+ slowly depolarizes nodal cells -> this will become pacemaker potential in nodal cells (This will create If)
  • HCN does not inactivate
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11
Q

II. Mechanism of pacemaker potential
5/ What are the characteristics of T-type VGCC?

A
  • Initial depolarization begins when the pacemaker potential reach around -45mV -> T-type VDCC opens and allows some Na+ and Ca2+ to come in
  • It will close when the membrane potential reach around -25mV
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12
Q

II. Mechanism of pacemaker potential
6/ What are some characteristics of L-type VGCC?

A
  • Activated when the membrane potential reach -25 mV (after the closing of T-type VGCC)
  • An influx of Ca2+ further depolarizes the membrane until the membrane potential reach 20 mV
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13
Q

II. Mechanism of pacemaker potential
7/ What are the characteristics of VG K+ channels?

A
  • At the peaks, various VGKCs open
  • They allow an outflow of K+ channels, repolarizing the membrane potential
  • Meanwhile, the L-type VGCC closes
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14
Q

II. Mechanism of pacemaker potential
8/ What are the characteristics of G-protein coupled rectified K+ channels (GIRKs)?

A
  • Activated by PARA signal (ACh) through M2-receptors
  • Responsible for hyperpolarizarion in response to ACh from vagal N. stimulation
  • Lengthen the time for pacemaker to reach the threshold which leads to a decrease in heart rate
  • Molecular mechanism: PARA signal -> GIRKs open -> hyperpolarization -> decreased AP-firing -> decreased heart rate
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15
Q

III. Control of pacemaker activity
1. Which systems control the pacemaker activity?

A

PARA and SYM nervous system

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16
Q

III. Control of pacemaker activity
2. Autonomic heart activity
a/ How is pacemaker activity controlled in sympathetic heart activity?

A

SYM signal
-> positive chronotropic effect -> increased HR

17
Q

III. Control of pacemaker activity
2. Autonomic heart activity
b/ What is the molecular mechanism of pacemaker activity controlled in sympathetic heart activity?

A

Molecular mechanism:
- β1-AR (Gs) (NE) -> ↑[cAMP]
- Gs -> ↑adenylyl cyclase -> ↑[cAMP] -> ↑PKA -> HCN activated -> If↑-> I (Ca,L) ↑
- Increases the funny current, therefore increases the
rate of depolarization
-> Reaches threshold faster = time period between AP shorter = heart frequency↑

(SYM signal
-> positive chronotropic effect -> increased HR)

18
Q

III. Control of pacemaker activity
2. Autonomic heart activity
c/ How is pacemaker activity controlled in PARA heart activity?

A

PARA signal -> negative chronotropic effect -> decreased HR

R. vagus nerve innervates SA node => decreased conduction frequency
L. vagus nerve innervates AV node => decreased conduction velocity

19
Q

III. Control of pacemaker activity
2. Autonomic heart activity
d/ What is the molecular mechanism of pacemaker activity controlled in PARA heart activity?

A

M2 receptor (Gi)
1. Gi ->↓AC ->↓[cAMP] -> ↓PKA -> HCN not activated ->↓If +↑IK,ACh
2. Gβγ -> GIRKs open -> hyperpolarization -> ↓AP firing-> ↓HR
3. Increase in K+ leads to hyperpolarization
3. Decrease in Ca2+ channels = more depolarization needed to reach threshold
4. Threshold for AP is more positive = requires longer time to reach threshold

20
Q

III. Control of pacemaker activity
3. How can circulating hormones regulate pacemaker activity?

A
  • Hyperthyroidism => tachycardia (↑HR)
  • hypothyroidism => bradycardia (↓HR)
  • Circulating epinephrine -> tachycardia (similar mechanism to NE released by SYM)
21
Q

III. Control of pacemaker activity
4. Drugs
a/ An example of a drug that can cancel PARA effect. Provide details about its mechanism

A

Cancelling PARA effects with the M2-receptor blocker atropine increased HR by about 50 bpm

22
Q

III. Control of pacemaker activity
4. Drugs
b/ An example of a drug that can cancel SYM effect. Provide details about its mechanism

A

Cancelling SYM effects with β1-receptor blocker propanol only decreases the HR by about 10 bpm

23
Q

III. Control of pacemaker activity
4. Drugs
c/ What happen of we use both β1-receptor blocker propanol and M2-receptor blocker atropine?

A

Using both drugs produced a HR of about 100bpm, the intrinsic pacemaking frequency of the SA node

24
Q

IV. Extra
1. What happens if the pacemaker activity of the SA node fails?

A
  • The other cells in the conducting system can also initiate pacemaker potential as they also contain HCN channels
  • The region with the highest rate of depolarization (intrinsic frequency) can take over the pacemaker activity, in case of SA node failure

A Physiology (88 decks)

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