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Cardiovascular System > Cardiac Contraction > Flashcards

Cardiac Contraction Flashcards

1
Q

What ion is responsible for cardiac contraction?

A

Rise in [Ca2+]ᵢ is central to contraction

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2
Q

Summarise how cardiac contractions occur

A

0) Na+ channels open allowing Na+ to enter and
depolarise cell

2) Plateau phase due to Ca2+ influx and CICR
- force of contraction is proportional to [Ca2+]ᵢ

3) Ca2+ channels close and K+ channels fully open
causing K+ to leave and repolarise cell causing muscle
relaxation

4) Stable Na+/K+ ATPase - 3 Na+ out for every 2 K+ in

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3
Q

Approximately what is the Diastolic [Ca2+]ᵢ ?

A

0.1 µM

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4
Q

What is the normal and maximum systole [Ca2+]ᵢ ?

A

Can rise to 1.0 µM to a maximum of 10.0 µM

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5
Q

How long does an action potential last?

A

200 - 500 ms

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6
Q

What causes cardiac myocyte contraction?

A

Electrical excitability contracts cardiac myocytes

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7
Q

Explain how [Ca2+]ᵢ affects cardiac contraction?

A

Contraction is determined by increases in [Ca2+]ᵢ

Higher increases in [Ca2+]ᵢ . increases contraction force

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8
Q

What are T tubules?

A

invaginations of the sarcolemma that penetrate into the centre of myocytes

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9
Q

What is the sarcoplasmic reticulum?

A

A membrane bound structure which stores Ca2+ in muscle cells, similar to ER

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10
Q

What is a Ryanodine Receptor?

A

Intracellular Ca2+ channel

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11
Q

Explain how cardiac contraction occurs in myocytes on a molecular basis

A
  1. Action potential (Na+ ions) depolarise T tubules,
    activating VGCCs causing Ca2+ influx
  2. Ca2+ binds to RyR on SR
  3. Release of Ca2+ from SR causing CICR
  4. Ca2+ binds to troponin, displacing the troponin-
    tropomyosin complex to activate the actin active site
  5. Myosin thick filament head binds to actin active site
  6. Myosin head ATPase activity releases energy
    (ATP -> ADP) allowing filaments to bind
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12
Q

Why does an increase in [Ca2+]ᵢ cause more contractility?

A

Rises in [Ca2+]ᵢ causes more actin-myosin interactions as more actin active sites are exposed so more cross-bridges can form = more contractility

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13
Q

What is the role of troponin?

A

Troponin regulates tropomyosin conformation

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14
Q

Describe the structure of troponin

A

Troponin composed of 3 regulatory subunits

  • TnT : troponin T binds to tropomyosin
  • TnI : troponin I binds to actin filaments
  • TnC : Troponin C binds to Ca2+
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15
Q

What affect does [Ca2+]ᵢ have on Troponin?

A

Binding of Ca2+ to TnC causes conformational changes in tropomyosin, exposing actin binding sites

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16
Q

What are the specialised roles of TnI and TnT?

A

TnI and TnT are important blood plasma markers for cardiac cell death (e.g. following MI)

17
Q

What does a decrease in [Ca2+]ᵢ cause?

A

Muscle relaxation

18
Q

Explain how cardiac muscle relaxation occurs?

A
  1. Action potential repolarisation (K+ influx) repolarises T
    tubules causing closure of VGCCs and Ca2+ influx
  2. No Ca2+ influx so no CICR
  3. Extrusion of Ca2+ from cell
    - 30% by Na+/Ca2+ exchanger
    - 70% by SR uptake via SR membrane Ca2+ ATPase
  4. Uptake of Ca2+ in mitochondria via importer
19
Q

How does Starling’s Law affect contractility?

A

Increased Pressure / Volume causes increased SV and intrinsic stretch. Even at the same pressure / Volume, contractility can increase (inotropic effect)
Extrinsic effect due to rise in [Ca2+]ᵢ

20
Q

Clinically what are most drugs related to contractility used for?

A

In the clinic, drugs mostly needed to increase contractility of heart, mostly to correct acute / chronic heart failure

21
Q

How do drugs increase [Ca2+]ᵢ ?

A
  1. Increase VGCC activity (sympathetic mimetic)

2. Reduce Ca2+ extrusion (Cardiac glycosides)

22
Q

How does the sympathetic nervous system affect contractility?

A

ꞵ₁ adrenoceptors increase contractility and are found on contractile cells of the heart (atrial / ventricular cells)

23
Q

Outline the effects of the sympathetic nervous system on contractility

A
  1. Noradrenaline binds to ꞵ₁ adrenoceptors stimulating Gs
    sub unit
  2. Activates adenyl cyclase which activates cAMP
  3. cAMP phosphorylates PKA, phosphorylating VGCCs,
    increasing Ca2+ channel activity
  4. Ca2+ influx causes CICR
  5. Myosin-actin interactions increase contractility
24
Q

What are the effects of increased PKA?

A
  • Increased Ca2+ channel activity - higher [Ca2+]ᵢ = more
    contractions
  • Increased K+ channels open -> faster repolarisation so
    shorter action potentials and faster HR
  • Increased SR Ca2+ ATPase - Ca2+ uptake into SR
    storage for faster relaxation
  • Overall stronger and faster contractions but diastolic
    time for filling with blood and coronary perfusion
    remains same
25
Q

What is the effect of cardiac glycosides?

A

Posiitive inotropic action of heart

26
Q

Explain how Digoxin increases contractility

A

Digoxin reduces Ca2+ extrusion

27
Q

What is Digoxin used for?

A

Chronic heart failure

-> reduced use now due to side effects

28
Q

Outline the mechanism of action of Digoxin

A
  1. Digoxin inhibits Na+/K+ ATP pump
  2. Build up of [Na+]ᵢ
  3. Less Ca2+ extrusion by Na+/Ca2+ Exchanger
  4. More Ca2+ uptake into stores - greater CICR
29
Q

Give examples of inotropic agents

A 
Digoxin 
Dobutamine 
Dopamine 
Glucagon 
Amrinone
30
Q

When are Dopamine and Dopabutamine used?

A

ꞵ₁ adrenoceptors stimulants used in acute heart failure

31
Q

What is the effect of Glucagon on the heart?

A

Glucagon acts as a GPCR stimulating the Gs pathway
increasing cAMP & PKA activity
Used for patients with acute heart failure taking ꞵ blockers

32
Q

What is the role of Amrinone on the heart?

A

Amrinone is a Heart specific Type III phosphodiesterase inhibitor (PED 3)
PDE reduces cAMP levels and PKA activity by converting cAMP to AMP, reducing contractility

33
Q

What is the effect of PDE inhibition?

A

PDE inhibition leads to a build up of cAMP activating PKA to phosphorylate VGCCs and increasing Ca2+ influx.

Only used in severe cases
e.g. patients on heart transplant waiting list

Cardiovascular System (16 decks)

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