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23 Cards in this Set
- Front
- Back
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1. During excitation contraction coupling in cardiac cells, what happens when one cardiac cell is activated?
How are cardiac muscle contractions triggered? What is the first event in excitation contraction coupling? |
When activate one cardiac cell, you activate all
Triggered by electrical signals from neighboring cardiac muscle cells First event - L type Ca channels (on T tubules) open **these are voltage-gated channels |
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2. In which direction does the Ca diffuse?
What role do the T tubules have in the excitation contraction coupling? (two things) |
From outside to the inside of the myocyte down its concentration gradient
**10,000 x higher [Ca] outside cell than inside 1. Facilitate diffusion of Ca from extracellular space to site on L type Ca channels 2. Carry AP deep into interior of thick cardiac myocytes |
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3. Once the Ca enters through the L type Ca channels, what does it do?
(two things) What is the "calcium induced calcium release"? |
1. Diffuse short distance
2. Binds to ryanodine receptors on sacroplasmic reticulum (SR) When Ca binds to RyR the Ca channels on the SR open Ca diffuses out of the SR b/c there is higher [Ca] inside SR than in cytoplasm **Ca induced Ca release from SR greatly increases intracellular [Ca] |
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4. How does the source of Ca differ in cardiac muscle from skeletal muscle?
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Skeletal muscle - only get Ca from SR
Cardiac muscle - also get Ca diffusing across so can regulate intracellular [Ca] through sympathetic |
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5. How is the beginning of the cross bridge cycle initiated?
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Some of the Ca binds to the troponin C molecule
Upon binding a conformational change occurs in tropomyosin molecule - it moves exposing the binding site Myosin cross bridge can attach to actin molecule binding site |
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6. What are the five steps in the cross bridge cycle?
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1. Active-site exposure
**tropomyosin moves out of way when Ca binds to TnC 2. Cross-bridge formation 3. Pivoting of mysoin head **cross bridge swivels 4. Cross-bridge detachment 5. Myosin reactivation |
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7. What happens when the cross bridge swivels or pivots?
What does this cause? What does the detachment of the cross bridge require |
R-1 and actin molecule move to left
Causes shortening b/c pull thin molecule into center of sacromere (towards center) Requires ATP binding to cross bridge |
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8. Is the muscle relaxing when the cross-bridge de-attaches?
What happens if you cannot get the cross bridge to de-attach? |
Muscle is not relaxing b/c it will go through this process thousands of times
Heart will get stiff and cannot fill properly so can pass out |
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9. What happens during the relaxation of the cardiac myocytes?
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1. L type Ca channels close
(closed by Ca itself) 2. Ca channels on SR close 3. Ca is pumped by active transport via SERCA molecules back into SR **reduce intracellular [Ca] |
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10. What does the SERCA molecule use?
Is relaxation an active or passive process? Why is relaxation of cardiac myocytes necessary? |
Uses ATP for energy
Relaxation takes a lot of energy (active process) Need relaxation b/c this is the time when the heart fills |
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11. How is SERCA normally?
How is SERCA assisted so that is does not have to pump against such a high concentration gradient? |
Normally somewhat inhibited by protein phospholamban
Protein calsequestrin binds CA w/in SR and helps to reduce the concentration of free Ca w/in SR |
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12. How is Ca pumped out of the cell?
How is this type of transport compared to SERCA? How is this pump pumping Ca? Where does it derive its energy from? |
By the Na-Ca exchanger (NCX)
Indirect active transport (doesn't require ATP) Pumping Ca against concentration gradient so needs energy Energy |
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13. How is SERCA normally?
What assists SERCA so that is does not have to pump against such a high concentration gradient? |
SERCA is normally somewhat inhibited by protein called phospholamban
Calsequestrin binds Ca w/in the SR and helps reduce the concentration of free Ca w/in the SR |
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14. How is Ca pumped out of the cell?
What type of transport is this? How is Ca pumped by this transport system? Where does the energy for this come from? |
Pumped out of the cell by the Na-Ca exchanger (NCX)
Indirect active transport (doesn't use ATP) It pumps Ca against it's concentration gradient so it needs energy Energy comes for [Na] gradient (electrogenic pump) **pump Na in and Ca out |
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15. How is the Na pumped out of the cell?
What happens when the intracellular [Ca] decreases? |
Pump Na out w/ Na/K pump which uses ATP directly
1. Ca no longer binds to troponin 2. Myosin binding site on thin filament is covered by tropomyosin 3. Myosin cross bridges detach and force generation stops |
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16. What happens if you block the Na/K ATPase?
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[Na] gradient decreases so Na-Ca exchanger rate will decrease
Less Ca pumped out Intracellular [Ca] will not lower so bound to TnC |
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17. Since relaxation requires energy, what happens if ATP is no longer available?
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Hear will not relax properly
Lack of coronary blood flow can result in inadequate ATP concentration Heart cannot relax properly it's filling w/ blood may be reduce b/c heart muscle is stiff (i.e. low compliance) Can't eject blood properly |
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18. What is a major determinant of the force of cardiac contraction?
How is the relationship? How is the intracellular [Ca] regulated? What is the NT? When is there an increase in contractility or inotropic state? |
Intracellular [Ca]
As [Ca] increases, force increase **not linear relationship though Sympathetic nervous system Norepinephrine **binds to adrenergic receptor beta 1 When intracellular [Ca] increases and force of contraction increases |
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19. What happens to the L type Ca channels when there is sympathetic activation?
What happens to phospholamban? What does SERCA do as a result? What ultimately happens to the duration of the contraction? |
Phosphorylated which allows more Ca to enter the cell and increases the force of contraction (increase in contractility)
Protein is phosphorylated which decreases its inhibition of SERCA Less SERCA inhibition causes SERCA to pump Ca more quickly back into the SR Shorten the duration of contraction so heart can relax quicker and preserve time for filling |
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20. How are cardiac contraction and duration of heart relaxation related?
When does the heart fill w/ blood? How are heart rate and duration of heart cycle related? Why is more rapid relaxation desirable? |
Decreasing time for cardiac contraction increases the time during which the heart is relaxed
During the time the heart is relaxed it fills w/ blood As heart rate goes up duration of heart cycle goes down Want more rapid relaxation to ensure contralateral filling **have more time for filling |
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21. In order to increase sacromere length above it equilibrium what must be applied?
What is the equilibrium length of the sacromere? What does the active length-tension relationship demonstrate about sacromere length and force? |
External force
Its length when it is relaxed and when there is no external force applied to it When the sarcomere length is increased the amount of force developed by the sarcomere is increased |
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22. Why does sarcomere force development increase as sarcomere length is increased?
What happens to the force necessary to stretch the sarcomere length when the heart is relaxed (no cross-bridge cycle)? |
B/c of the change in overlap of the thick and thin filaments
Takes more force to stretch sarcomere length |
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23. How can contraction be increased?
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1. Sympathetic activation
2. Sarcomere length **stretch more = more force **sarcomere gets longer and it can develop more force |
