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Undeleted > Lecture 10: Excitation-Contraction Coupling (Hayward) > Flashcards

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
Q

How does external Na concentration effect RMP?

A

It doesn’t. RMP is independent of this (depends mainly on K)

26
Q

What DOES Na+ concentration influence in heart?

A

AP, contractility

27
Q

Decreased Na outside cell –> conc. Ca inside cell?

A

increased

28
Q

Increased Na inside cell –> conc. Ca inside cell?

A

increased

29
Q

What is rate of heart relazation most dependent on?

A

how quickly Ca++ can be re-sequestered

30
Q

Methods of cytosolic C++ release

A

1) extracellular influx through Ca channels
2) Ca triggered Ca release from SR
3) Na/Ca exchanger

31
Q

Methods of cytosolic Ca decrease

A

1) SR reuptake
2) Ca ATPase pump on sarcolemma
3) Na/Ca exchanger

32
Q

transverse tubule system

A

invaginations of sarcolemma which help transfer the AP to the inner part of the muscle membrane. Most prominent in ventricular muscle and atria muscle

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