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Physiology 1 > Cardiac contraction > Flashcards

Cardiac contraction Flashcards

1
Q

What is the diastolic concentration of calcium within a cardiac cell?

A

Diastolic [Ca2+] 0.1 μ M

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2
Q

What does the [Ca2+] rise to during systole? ̴

A

Normal systole [Ca2+] may rise 1 μM

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3
Q

What does the [Ca2+] rise to if the cardiac cell is contracting at its hardest?

A

Maximum systole [Ca2+] may rise ̴10 μM

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4
Q

How does an action potential travel into a cardiac cell?

A

It travels through the t-tubule system

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5
Q

What are t-tubules?

A

Invaginations of the sarcolemma that penetrate into the cardiac muscle cells

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6
Q

What happens when the action potential enters the cardiac cell?

A

Causes voltage gated calcium channels to open leading to the influx of calcium ions from the t-tubule into the cardiac muscle cell

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7
Q

What membrane potential is needed for the voltage gated calcium channels to open?

A

30 – 40mV

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8
Q

Where does the calcium bind to once released?

A

Binds to the Ryanodine receptors within the Sarcoplasmic reticulum membrane

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9
Q

What happens as a result of calcium binding to the ryanodine receptors?

A

Causes them to open leading to calcium to be released from the sarcoplasmic reticulum into the cytoplasm of the cardiac cell

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10
Q

What is the process of calcium binding to the ryanodine receptors and casing calcium release called?

A

Calcium induced calcium release (CICR)

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11
Q

Why don’t you need a large influx of calcium to open the ryanodine receptors?

A

Because the influx of calcium from the t-tubules occurs in such a small area it means that although the “amount” of calcium is small the conc. of calcium delivered to the ryanodine receptors is quite high - high enough to open the receptors

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12
Q

What occurs after calcium has been released into the cardiac cell via calcium-induced calcium release?

A

Calcium then binds to the Troponin-C subunit on the troponin causing a conformational change in the troponin-tropomyosin complex.

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13
Q

Why is the conformational change in the troponin-tropomyosin complex necessary for cardiac contraction?

A

Because it causes tropomyosin to be moved away from the myosin head binding sites on the actin thus exposing these binding sites to the myosin head.

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14
Q

What happens once the tropomyosin is moved away from the actin?

A

Myosin head binds to actin causing formation of cross bridge. Myosin head then produces power stroke thus shortening the sarcomere.

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15
Q

Explain all the steps involved in the contractile cycle

A
  1. binding of Ca2+ to troponin-C subunit on troponin causes conformational change causing tropomyosin to be moved away from the myosin head binding sites on the actin thus exposing the myosin head binding sites on the actin.
  2. Myosin head then binds to actin causing the formation of a cross bridge
  3. ADP is then released from myosin head causing myosin molecule to undergo a conformational change leading to power stroke - Power stroke causes Actin to be moved over the myosin thus leading to shortening of the sarcomere
  4. Once power stroke over ATP molecule binds to myosin head causing myosin head to detach from the actin filament (cross-bridge dissociates).
  5. Inherent ATPase of myosin head then hydrolyses ATP to form ADP and inorganic phosphate. This causes cocking of myosin head
    Cocking of myosin head puts myosin head in position to bind to actin
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16
Q

Why is cardiac contraction described as calcium dependent?

A

Because without calcium myosin can’t bind to actin menaing no contraction. Also, not only is whether or not contraction occurs calcium dependent but also how hard the contraction is. This is because increase in Ca2+ means more myosin head binding sites exposed which means formation of more cross-bridges & greater contractility.

17
Q

What are the 3 regulatory subunits that make up troponin and what are their functions?

A 
Troponin T (TnT) - binds to tropomyosin
Troponin I (TnI) – binds to actin filaments
Troponin C (TnC) – binds Ca2+
18
Q

Give an example of a diagnostic use of some of the troponin subunits?

A

Troponin I and Troponin T are important blood plasma markers for cardiac cell death because they can be released into the blood stream if for example someone has a heart attack. They can then be measured within the bloodstream.

19
Q

Explain the steps involved in cardiac myocyte releaxation

A
  1. Voltage gated potassium channels open leading to K+ ion influx causing repolarisation of T-tubules. Closure of Voltage-gated Calcium Channels also occurs which causes Ca2+ influx to decrease.
  2. Without Ca2+ influx there’s no Calcium Induced Calcium Release which means intracellular calcium levels remain very low.
  3. Calcium already in the cardiac myocyte cytoplasm is then pumped out of the cell by the Na+/Ca2 + exchanger (NCX).
  4. Ca2+ is also taken up into the Sarcoplasmic Reticulum via Sarco/endoplasmic Reticulum Ca2+ATPase (SERCA) – Ca2+ transported back to Sarcoplasmic Reticulum so it can be used for next contraction.
  5. Some calcium is also taken up by the mitochondria.
20
Q

How do all of these mechanisms cause the cardiac myocytes to relax?

A

These mechanisms cause a reduction in calcium concentration. This reduction in calcium concentration means that myosin can’t bind to actin thus preventing contraction of the cardiac muscle
This allows the chambers to relax and refill

21
Q

How much calcium within the cytoplasm of the cardiac myocyte is transported out of the cell by the Na+/Ca2 + exchanger?

A

30% of calcium within the cytoplasm leaves via this mechanism

22
Q

How much calcium within the cytoplasm of the cardiac myocyte is taken back up into the sarcoplasmic reticulum?

A

70% of calcium within the cytoplasm goes back to the SR

23
Q

What is the purpose of the calcium being taken back up into the SR?

A

Allows the calcium to be re-released from the sarcoplasmic reticulum for the next contraction. Also means calcium reserves within the SR don’t become depleted allowing contraction to occur whenever it’s needed.

24
Q

What is the effect of an increase in Ca2+ on the energy of contraction?

A

It increases contractility without a need for a pressure or volume increase. Classed as an inotropic effect because calcium increases the strength of cardiac muscle contraction.

25
Q

What are the 2 main ways that the contractility of the heart can be increased clinically?

A
  1. Increasing Voltage Gated Calcium Channel activity – via sympathetic mimetic drugs which bind to B1 adrenoreceptors causing VGCCs to become more sensitive to voltage
  2. Reducing Ca2+ removal via cardiac glycosides
26
Q

Why are both sympathetic mimetic drugs and cardiac glycosides classed as postive inotropes?

A

Because they both increase the strength of cardiac muscle contraction by increasing the conc. of Ca2+ within the cardiac cell .

27
Q

Describe the process that means that the activation of B1-adrenoreceptors leads to an increase in contractility?

A
  1. Noradrenaline binds to B1-adrenorecptor causing the receptor to become activated
  2. Activation of B1-adrenoreceptors causes the αGs subunit to bind GTP instead of GDP
  3. GTP bound αGs subunit dissociates from rest of G-protein and activates the enzyme adenylate cyclase
  4. Adenylate cyclase then catalyses reaction that causes the formation of cAMP from ATP
  5. cAMP then activates protein kinase A
  6. Protein kinase A then phosphorylates voltage-gated Ca2+ channels causing them to become more sensitive to voltage - this means more Ca2+ moves into the cell once voltage needed to open the VGCC’s is reached
  7. Calcium binds to ryanodine receptors causing calcium to be released from SR (calcium induced calcium release)
  8. This calcium then interacts with actin/myosin leading to muscle contraction
28
Q

What does it mean for the voltage gated calcium channels when they become more sensitive to voltage?

A

It means that more of them will open at any particular voltage - This is any voltage above the voltage needed for them to open.

29
Q

What are the effects of phosphorylation by protein kinase A?

A
  1. Increases Ca2+ channel sensitivity to voltage so higher Ca2+ levels and greater contraction
  2. Increases K+ channel opening leading to more K+ flowing out of the cell. This causes faster repolarisation and shorter action potential…leads to faster heart rate
  3. Increases Sarcoplasmic Reticulum Ca2+ATPase uptake of Ca2+ into Sarcoplasmic Reticulum allowing faster relaxation
30
Q

What do these effects mean for the heart?

A

Overall these effects lead to stronger faster contractions but same diastolic time to allow for filling with blood & coronary perfusion.

31
Q

What is digoxin?

A

It’s an example of a positive inotrope. It increases contractility by reducing Ca2+ extrusion

32
Q

How does digoxin increase contractility?

A
  1. Digoxin inhibits Na+/K+ ATPase – this means Na+ can’t be transported to outside of cell
  2. This means that a Na+ concentration gradient isn’t built up so Na+ isn’t able to diffuse down this gradient to the inside of the cell from the outside via the Na+/Ca2+ ATPase but instead just build ups inside the cell.
  3. Without transporting Na+ the Na+/Ca2+ ATPase isn’t able to transport Ca2+ out of the cell
  4. This means instead of being transported out more Ca2+ is taken up into the sarcoplasmic reticulum and leads to greater Calcium Induced Calcium Release
33
Q

Name other examples of positive inotropes?

A

Dobutamine & dopamine - β1-adrenoceptor stimulants

Glucagon – acts at G protein coupled receptor, stimulates Gs pathway, increases cAMP and PKA activity.

Amrinone – a Type III phosphodiesterase inhibitor (PDE3 inhibitor)

34
Q

How does PDE3 reduce contractility?

A

PDE converts cAMP into AMP reducing cAMP and decreasing PKA activity – reduces contractility.

35
Q

How does a PDE3 inhibitor reverse the effects of PDE3?

A

PDE inhibition leads to a build-up of cAMP that activates PKA to phosphorylate Voltage Gated Calcium Channels and an increase in Ca2+ influx.

Physiology 1 (31 decks)

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