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sem 2 > Cardiac contraction > Flashcards

Cardiac contraction Flashcards

1
Q

Define Cardiomyoctyes? (2pts)

A
  1. Cardiomycotyes are 60-140 um in length and 17-25um diameter which make up the branching myofibrils. Each myoctye contains multiple. rod-like cross-banded strands (myofibrils) that run the length of the cell and are composed of repeating sacromeres.
  2. Th cytoplasm between the myofibrils contains the single centrally located nucleus, mitochondria and sarcoplasmic reticulum.
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2
Q

How do sarcomeres cause muscle contraction? (1pts)

A

Sacromeres cause muscle contraction when actin and mysoin filaments move relative to each other.

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3
Q

Describe a cardiomyoctyes function?

A
  1. The t-tubules ( invaginations of the membrane) have calcium channels and ensure calcium is delivered deep into the cell close to the sarcomere
  2. Ca2+ enters via calcium channels that open in response to the wave of depolarization that travels along the sarcolemma where they trigger the release of more calcium from the sarcoplasmic reticulum and intiate contraction.
  3. The actin-mysoin overlap is shown for systole when Ca2+ is maximal and diastole when Ca2+ is minimal.
  4. Eventually the Ca2+ that has entered the cell leaves predominately through a Na+/ Ca2+ exchanger.
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4
Q

What is a stable Na/K+ pump?

A

3Na+ out and 2K+ in

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5
Q

What is contraction determined by?

A

Contraction is determined by an increase in calcium concentration. The amount of calcium is proportional to the force of contraction. An increase in calcium ions increases the force of contraction.

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6
Q

What does action potential do?

A

Action potential causes cell depolarisation which opens calcium channels

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7
Q

Define T-tubules

A
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8
Q

Define T-tubules

A

Invaginations off the cell membrane that penetrate into the centre of the cardiac muscle cell. They contain calcium channels and ensure calicum is delivered deep into the cell close to the sarcomere

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9
Q

Define the sarcoplasmic reticulum?

A

Membrane bound structure within muscle cells similar to the endoplasmic reticulum in other cells and stores Ca2+

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10
Q

Describe the intra- cellular rise in Calcium ions? (4pts)

A
  1. Action potential depolarises T tubules and activates voltage gated calicum channels causing Ca2+ influx
  2. Ca2+ binds to Ryanodine receptos which is located on the SR
  3. The SR releases calcium ions. Calcium induced calcium release then occurs increasing intracellular levels of calcium ions
  4. Calcium ions then bind to troponin. The displacement of tropmyosin/ troponin complex occurs exposing active sites on actin
  5. Mysoin thick filaments head binds to the active site on actin and filaments slide using ATP.
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11
Q

Describe how the rise in Ca2+ ions initiates contraction? (5pts)

A
  1. Calcium binds to troponin c which changes conformation of tropomyosin exposing actin binding sites
  2. Hydrolysis of ATP causes myosin to extend and bind head to actin forming cross bridges.
  3. Power stroke moves actin filament relative to myosin. ADP and Pi is released from the mysoin heads
  4. Myosin remains attached to actin until a new molecule of ATP binds
  5. The cycle continues until cellular calcium levels decrease allowing calcium to dissociate from troponin which returns to the original confirmation which blocks actin binding site.
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12
Q

Describe the Troponin-Tropomysoin complex? ( 4pts)

A
  1. Troponin regulates the confirmation of tropomysoin
  2. Troponin is made up of 3 regulatory subunits:
  3. Troponin T ( TN T) - binds to tropomysoin
  4. Troponin I ( TN I) – binds to actin filaments
  5. Troponin C ( TN C) – binds to Ca 2+ channel
  6. Binding of Ca2+ to TNC leads to conformation chnages of tropomysoin and exposure of actin binding sites
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13
Q

Why are TNI and TnT important?

A

TnI and TnT are important blood plasma markers for cardiac cell death

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14
Q

Describe decrease in Ca2+ ions and relaxation? (4pts)

A
  1. Action potential repolarisation ( K+ ions leave) repoalrises T-tubules. The closure of voltage dependant calcium channels occurs and there is a decrease in the concentration of calicum ions
  2. There is no calcium ions influx. No CICR
  3. Calcium ions are released from the cell by a Na+/ cA2+ exchanger.
  4. Calcium ions uptake into the SR via the SR membrane occurs. Calcium ions enter SR for the next contraction even relation requires ATP
  5. The uptake of calcium ions occurs in the mitochondria
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15
Q

What happens when the concentration of Calcium increases? (2pts)

A
  1. As the concentration of calcium increases the stroke volume increases
  2. The same intrinsic stretch is kept.
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16
Q

Describe how drugs affect the contractility of the heart?

A
  1. In the clinic drugs are needed to increase contractility of the heart
  2. It is mostly used to correct heart failure
  3. The aim of the drugs is to increase calcium ions by:
  4. Increasing the voltage gated calcium channel activity
  5. Reducing calcium extrusion ( cardiac glycosidase)
17
Q

How does the sympathetic nervous system release noradrenaline?

A

The sympathetic nervous system releases noradrenaline which acts on beta 1 adreno-receptors to increase the contractility of the heart by phosphorylating the voltage gated calcium channels. When they are phosphorylated they open more easily and more of them open. An increase in intracellular calcium occurs which causes an increase in stroke volume.

18
Q

How do B1-adrenorecprotrs induce increased contractility? (6pts)

A
  1. Noroadrenaline binds to a Beta 1 receptor. Beta1 adrenergic receptors are found on the contractile cells of the heart, the atrial and the ventricular cells
  2. This triggers adrenaline cyclase and causes ATP to become cyclic AMP
  3. This increases cyclic AMP inside the cell and activates protein kinase A
  4. Protein kinase A phosphorylated the receptors and the voltage gated calcium channels
  5. When an action potential arrives at the channels they open much more easily and more of them open for longer.
  6. A calcium influx occurs. Increased contractility occurs
19
Q

What does increased protein Kinase A lead to? (4pts)

A
  1. Increased calcium channel so higher Ca2+ levels and greater contraction
  2. Increased K+ channel opening so faster repolarisation and a shorter action potential occurs. This leads to a faster heart rate
  3. Increased sarcoplasmic reticlum Ca2+ ATPASE so uptake of Ca2+ storage by SE allowing faster relaxation
  4. Overall storage faster contractions but must have the same diastolic time to allow for filling with the blood and coronary perfusion.
20
Q

What is Digoxin?

A

Dixogin is a drug used for chronic heart failure. It increases contractility by reducing Ca2+ extrusion. It is no longer used as much due to side effects.

21
Q

How does Digoxin work? (4pts)

A
  1. Digoxin inhibits the Na+/ K+ pump
  2. The build up of Na+ lowers the concentration gradient which normally powers Na+/ Ca2+ exchanger
  3. There is less Ca2+ expulsion by Na+/ Ca2+ exchanger.
  4. There is more Ca2+ uptake into stores and greater calcium induced calcium release.
22
Q

Describe the role of Glucagon? (3pts)

A
  1. Acts as a G protein coupled receptor
  2. Stimulates the G pathway
  3. Increased cAMP and PKA activity
  4. used in patients with acute heart failure who are taking B-blockers
23
Q

Describe the role of Amrionone

A

A phosphodieaster inhibitor which converts cyclic AMP into AMP

sem 2 (12 decks)

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