Lecture 10: Excitation-Contraction Coupling (Hayward) Flashcards

1
Q

What triggers myocardial force production?

A

Ca influx via channels in sarcoplasmic reticulum. Ability of heart to contract is influenced by extracellular conc. of Ca

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2
Q

What do actin/myosin need to contract?

A

Ca (takes away an inhibition that prevents their interaction)

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3
Q

What is essential for intracellular Ca++ release?

A

Extracellular Ca release

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4
Q

What terminates Ca influx?

A

repolarization

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5
Q

duration of AP is fx of:

A

speed of Ca channels

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6
Q

What triggers relaxation of myocardial muscle?

A

Activation of Ca/ATPase Pump by phosphorylation of phospholambin

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7
Q

What trigger phosphorylation of phospholambin? (2)

A

Increases in intracellular Ca++

Increases in cAMP levels

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8
Q

Calmodulin

A

Inhibits further Ca release as Ca/ATPase is activated to get rid of Ca and relax cardiac muscle

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9
Q

Ca/ATPase

A

pump that removes Ca into extracellular space to induce muscle relaxation. Activated by phosphorylation of phospholambin. Inhibited at rest

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10
Q

Why is it important to start reuptaking Ca as soon as its released?

A

To ensure duration of contraction follows period of depolarization only

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11
Q

3 main mechs of Ca removal:

A

1) Na/Ca exchanger and Ca pump in the plasma membrane both extrude Ca from space into extracellular space (80%)
2) Ca pump sequesters Ca within SR
3) Ca is bound in the SR by calreticulum and calsequestrin

2+3 = 20%

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12
Q

What does digitalis drug manipulate

A

inhibits Na/K ATPase, causing buildup of intracellular Na and decreasing concentration gradient for Na/Ca exchanger

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13
Q

Where is MOST Ca sequestered?

A

SR

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14
Q

Na/Ca exchanger**

A

Forces 1 Ca++ out, 3 Na+ into cell **

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15
Q

Force production in cardiac vs. skeletal muscle

A

skeletal —> by changing numbers of AP to muscle over a period of time (more AP = more force)

cardiac –> change intracellular Ca concentrations (more Ca = stronger/longer AP)

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16
Q

Mechanisms that can raise or lower intracellular Ca concentration can therefore modulate:

A

contractile force/systolic force production in heart

17
Q

How to increase heart contractility?

A

bring more Ca into cell from surface and release more into cell from SR

18
Q

very high Ca concentration can induce:

A

cardiac arrest in systole (muscle can’t relax)

19
Q

What parts of heart does sympathetic system affect? ***

A

SA node, AV node, cardiac tissue ***

20
Q

What parts of heart does parasympathetic system affect? ***

A

Pacemaker cells ***

21
Q

What receptor activation increases Ca opening in myocardial cells?

A

beta-1 (via SYMPATHETIC stimulation)

22
Q

sympathetic effect on Ca release and sequestration

A

Quickens release AND reuptake of Ca. Increases contractility.

23
Q

Parasympathetic effect on Ca release and sequestrian

A

little direct effect

24
Q

time-dependent accumulation of Ca

A

increases in HR result in more Ca influx and less time for Ca removal

25
How does external Na concentration effect RMP?
It doesn't. RMP is independent of this (depends mainly on K)
26
What DOES Na+ concentration influence in heart?
AP, contractility
27
Decreased Na outside cell --> conc. Ca inside cell?
increased
28
Increased Na inside cell --> conc. Ca inside cell?
increased
29
What is rate of heart relazation most dependent on?
how quickly Ca++ can be re-sequestered
30
Methods of cytosolic C++ release
1) extracellular influx through Ca channels 2) Ca triggered Ca release from SR 3) Na/Ca exchanger
31
Methods of cytosolic Ca decrease
1) SR reuptake 2) Ca ATPase pump on sarcolemma 3) Na/Ca exchanger
32
transverse tubule system
invaginations of sarcolemma which help transfer the AP to the inner part of the muscle membrane. Most prominent in ventricular muscle and atria muscle