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Cardiovascular System Module > Lecture 8 -control And Regulation Of Contraction > Flashcards

Lecture 8 -control And Regulation Of Contraction Flashcards

1
Q

How do you measure strength?

A

You look at the volume of blood that is ejected

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2
Q

What does the sympathetic nervous system do to the heart?

A

Increases heart rate as it innervates the nodes of the cell

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3
Q

What do the right sympathetic nerves do?

A

Innervates the SA node and causes the heart rate to go up

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4
Q

What is a positive chronotropic affect?

A

Increase in heart rate

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5
Q

What do the left side of the sympathetic nerves do?

A

Innervates the ventricular muscle which increases the stroke volume (increasing contractility)

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6
Q

What does the parasympathetic nervous system do to the heart?

A

Decreases heart rate

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7
Q

What does the right side of the parasympathetic nerves do?

A

Innervates the SA node

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8
Q

What does the left side parasympathetic nerves do?

A

Innervates the AV node

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9
Q

Can parasympathetic innervation happen in the ventricular muscle?

A

No only in the nodal tissues

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10
Q

What is a negative chronotropic affect?

A

Decrease in heart rate

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11
Q

What type of receptors do sympathetic nerve cells have?

A

Beta 1 receptors

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12
Q

What does sympathetic stimulation do to the regulation of heart rate?

A

Depolarises the SA node and increases the rate of depolarisation - depolarises the pacemaker of the cell

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13
Q

What happens when the rate of depolarisation increases?

A

Calcium channels are opened quicker as you have reached the threshold more quickly - more action potentials

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14
Q

What receptors are involved in the parasympathetic regulation of heart rate? And what is the neurotransmitter involved?

A

M2 muscarinic receptors and acetylcholine

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15
Q

What does parasympathetic stimulation do to the SA node (pacemaker)?

A

Hyperpolarises the cell and slows the heart rate - membrane potential becomes more negative

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16
Q

What happens when there is a slower depolarisation?

A

Means it takes longer to reach the threshold so the calcium channels don’t open as quick which decreases the heart rate

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17
Q

What drug blocks the muscarinic receptors?

A

Atropine

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18
Q

What does Adenylyl cyclase reduce?

A

Cyclic AMP and produces PKA

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19
Q

What does PKA phosphorylate?

A

The voltage operating calcium channel (VOC) so ca2+ channels activate quicker

20
Q

What protein is the muscarinic receptor linked to?

A

GI protein which inhibits Adenylyl cyclase

21
Q

What happens to the betagamma subunit in the parasympathetic system?

A

The betagamma subunit separates from the alpha subunit and the alpha subunit goes off in the membrane and binds and activates the K+ channel

22
Q

What happens when the K+ channel is activated by the alpha subunit?

A

The k+ ions leave the cell and the cell repolarises which is why the parasympathetic stimulation hyperpolarises the SA and AV node

23
Q

Why in the sympathetic response are the intracellular mechanisms more gradual?

A

Because cAMP levels have to build up, little NE is released during each cardiac cycle

24
Q

What is the sympathetic response unable to do?

A

To alter the cardiac behaviour very much within one cardiac cycle

25
Q

Why is the parasympathetic response rapid?

A

Because of the direct activation of K+ channels by betagamma subunit (there is no second messenger required)

26
Q

What are vagus nerves able to do in the parasympathetic response?

A

Able to exert beat-by-beat control of heart rate - removal of vagus results in increase in heart rate

27
Q

What stimulation dominates at rest?

A

The parasympathetic

28
Q

Extrinsic contraction?

A

Outside influence on the muscle cells e.g. neurotransmitter or a hormone causes contractility

29
Q

Intrinsic contraction?

A

Inherent in the muscle cells, a unique property of cardiac muscles in the cell

30
Q

Positive inotropic effect?

A

Increase stroke volume

31
Q

Positive chronotropic effect?

A

Increased heart rate

32
Q

What is an increase in contractility associated with?

A

An increase in ca2+ ion concentration - have to have more calcium ions as calcium ions trigger contraction

33
Q

What happens when there is an increased strength of contraction from a build up of pressure?

A

Stroke volume goes up

34
Q

How does activation of beta 1 receptors result in more calcium and stronger contraction?

A

Because PKA phosphorylates the voltage operating calcium channel so you get more trigger ca2+ which means more CICR and stronger contractions

35
Q

More CICR and stronger contractions =?

A

Stroke volume increases and contractility increases

36
Q

What needs to happen for the muscle to relax?

A

Cytoplasm needs to get ride of ca2+ which occurs by sympathetic stimulation when PKA phosphorylates phospholamban

37
Q

What happens when phospholamban is phosphorylated?

A

It speeds up the SERCA pump and you get an increase rate of pumping the ca2+ ions back out the cytoplasm

38
Q

Where are RYR receptors located?

A

Underneath the calcium channels

39
Q

What does maximum sympathies stimulation =

A

An increase in HR and SV independently

40
Q

What are class 2 - beta blockers known as?

A

Negative inotropic

41
Q

What do class 5 - cardiac glycosides do?

A

Inhibit the Na+/K+ ATPase pump

42
Q

What happens when the Na+/K+ATPase pump is inhibited?

A

Means the intracellular Na+ concentration rises in the cell which depolarises the cell

43
Q

How does the cell keep the Na+ levels normal when the Na/K+ ATPase pump is inhibited?

A

The Na/Ca exchanger reverses its led to get rid of the Na+ ions so Ca2+ will enter the cell - triggering a contraction

44
Q

What are class 5 - cardiac glycosides?

A

Positive ionotropes

45
Q

What is the mechanism for intrinsic regulation of stroke volume?

A

Frank-starling mechanism

46
Q

What does an increased filling pressure of the atria or the ventricles lead to?

A

An increase in end diastolic volume (the volume in the atria before contraction)

47
Q

What does an increase in filling pressure lead to?

A

An increase in EDV (end diastolic volume) which leads to an increase stretch int eh cardiac muscle which leads to an increase force of contraction

Cardiovascular System Module (18 decks)

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