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CVDM > Regulation of Cardiac Output > Flashcards

Regulation of Cardiac Output Flashcards

1
Q

What is cardiac output?

A

The amount of blood that the heart pumps through the circulatory system every minute

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2
Q

What equation gives cardiac output?

A

CO = HR x SV

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3
Q

True or false:
Cardiac output always remains the same

A

False
It varies - it changes in response to the body’s demand for oxygen

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4
Q

Give an example of a physiological process in which cardiac output increases

A

Exercise

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5
Q

What is the average value of cardiac output at rest compared to exercise?

A

Rest = 4.9 litres per minute
Exercise = up to 25 litres per minute (40 in athletes)

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6
Q

Why does cardiac output vary with exercise?

A

The demand for oxygen in the muscle and heart increases significantly with exercise

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7
Q

How does parasympathetic stimulation cause the heart to slow?

A

Vagal nerves to the heart increase the resting potential and decreases the rate of diastolic depolarisation

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8
Q

How does sympathetic stimulation increase heart rate?

A

Through the release of hormones (catecholamines - epinephrine and norepinephrine) which accelerate the heart rate

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9
Q

True or false - sympathetic stimulation also affects stroke volume

A

True - it increases the force of contraction thus increasing stroke volume

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10
Q

What 2 things influence stroke volume?

A

Sympathetic innervation and length-tension relationship of muscle fibres

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11
Q

What is stroke volume?

A

The volume of blood pumped by the heart per contraction

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12
Q

What 3 things determine the value of stroke volume?

A

Heart contractility
Preload
Afterload

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13
Q

What is preload?

A

The volume of blood in the heart at the end of diastole (end diastolic volume)

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14
Q

What is afterload?

A

The amount of pressure the heart requires to open the aortic valve

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15
Q

What is ejection fraction?

A

Fraction of blood in the left ventricle that is pumped out in each beat

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16
Q

Give the equation for ejection fraction

A

EF = (SV/EDV) x 100

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17
Q

What are the units for ejection fraction?

A

%

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18
Q

What does the Frank-Starling Relationship show?

A

The more the cardiac muscle is stretched, the greater the force the muscle exerts on contraction

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19
Q

What happens to the following with an increased EDV?:
Myocardium
Sarcomere length
Force of contraction

A

Myocardium becomes more stretch
Sarcomere length increases
Force of contraction increases

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20
Q

Increased stretch is caused by increased venous return which can be caused by what?

A

Increased skeletal muscle activity
Adrenergic effects of blood vessels (increased venous tone)
Respiratory pump (Increased depth and frequency of breathing)

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21
Q

How does a beta-1-adrenergic receptor agonist such as isoprenaline cause protein phosphorylation?

A

The beta-1-AR activates Gs, which increases cAMP via adenylate cyclase, which activates PKA which leads to protein phosphorylation

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22
Q

What are the meanings of the following words?:
- Inotropic
- Luisitropic
- Chronotropic

A

Inotropic - force of contraction
Luisitropic - rate of relaxation
Chronotropic - rate of contraction

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23
Q

What effect does isoprenaline (beta-1-agonist) have on the following:
- Calcium transients
- Twitches

A

Causes:
Bigger calcium transients
Bigger and faster twitches

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24
Q

Name some targets of PKA in cardiomyocytes?

A

Phospholamban
RyR
L-type Calcium Channel
Iks
Troponin I
Phospholemman

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25
Q

What is protein phosphorylation?

A

Reversible, post-translational attachment of phosphate groups to specific amino acids (Serine, Threonine, Tyrosine) within proteins

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26
Q

What is the common side chain in Serine, Threonine and Tyrosine?

A

Hydroxyl group

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27
Q

What adds phosphate groups to substrate proteins and what removes phosphate groups to substrate proteins during protein phosphorylation?

A

Added by protein kinases
Removed by protein phosphatases

28
Q

True or false:
At physiological pH the phosphate groups are negatively charged

A

True

29
Q

What are the two main types of protein kinase?

A

Serine/threonine kinases (e.g. PKA, PKC)
Tyrosine kinases (e.g. GFRs, EGF-R, PDGF-R)

30
Q

What group of protein kinases acutely controls cardiac output?

A

Serine/threonine kinases

31
Q

What are the major phosphates in the heart regulating cardiac output?

A

PP1
PP2A

32
Q

What does PP1 do?

A

Dephosphorylates phospholamban and ryanodine receptor

33
Q

What does PP2A do?

A

Dephosphorylates LTCC, ryanodine receptor and troponin I

34
Q

What determines protein kinase substrate specificity?

A

Whether or not a serine, threonine or tyrosine residue becomes phosphorylated

35
Q

What determines whether or not a serine, threonine or tyrosine residue becomes phosphorylated?

A

The surrounding amino acid sequence

36
Q

Describe the structure of PKA

A

Tetramer consisting of 2 catalytic and 2 regulatory sub-units

37
Q

True or false:
The catalytic subunits of PKA bind cAMP

A

False
The regulatory subunits bind cAMP which causes release of the catalytic subunits

38
Q

Apart from cAMP, what else do the regulatory subunits of PKA bind to?

A

A-kinase anchoring proteins (AKAP)

39
Q

What is the function of AKAPs?

A

Responsible for compartmentalisation of PKA and other signalling enzymes within particular cellular microdomains
Facilitate spatiotemporal regulation of cell signalling in response to cAMP generation

40
Q

What processes to cardiac AKAPs regulate?

A

Calcium influx
Release from and reuptake of calcium into SR
Myocyte repolarisation

41
Q

What is the function of the ryanodine receptor?

A

Calcium channels responsible for calcium reduced calcium release from SR

42
Q

What things influence the opening of ryanodine receptors?

A

Free cytosolic calcium and luminal calcium

43
Q

How does free systolic calcium open ryanodine receptors?

A

Calcium binds to cytosolic region causes channel opening and calcium release from SR

44
Q

How does luminal calcium open ryanodine receptors

A

Calcium binding to RyR on luminal side of SR enhances channel opening

45
Q

True or false:
Ryanodine receptors are located very close to T-type calcium channels?

A

False
Ryanodine receptors are located very close to LTCC

46
Q

Where are ryanodine receptors located?

A

In the SR membrane

47
Q

What is the region between the LTCC and RyR called?

A

Dyadic cleft

48
Q

In what ways may RyRs be regulated?

A

pH
Caffeine
Nitric oxide
Other proteins
Kinases

49
Q

How does acidosis regulate the RyRs?

A

Reduces channel opening

50
Q

How does caffeine regulate the RyRs?

A

Increases calcium sensitivity and increases channel opening

51
Q

Which isoform of RyR is found in the heart?

A

RyR2

52
Q

How many transmembrane domains do RyRs have?

A

6 transmembrane domains with hydrophobic loop buried within the membrane

53
Q

How does mAKAP regulate RyR activity?

A

mAKAP brings PKA into close proximity with RyR2
mAKAP recruits several other signalling molecules to RyR2

54
Q

What causes resetting of the RyR system?

A

PP2A bound to mAKAP dephosphorylating RyR and pDE4D3

55
Q

PDE4 expression is increased/reduced in heart failure?
What does this lead to?

A

Reduced
Leads to RyR hyperphosphorylation and excessive Ca-release from SR via leaky RyR

56
Q

What phase of the action potential is the voltage-gated calcium channel responsible for?

A

The plateau phase

57
Q

Where is the LTCC located?

A

Sarcolemma

58
Q

Function of LTCC

A

Entry of triggering calcium into myoocyte

59
Q

What regulates LTCC?

A

Channel opening occurs following membrane depolarisation which is facilitated by entry of Na into cell
Rad phosphorylation by PKA

60
Q

How does beta adrenergic stimulation cause an increase in LTCC activity?

A

Through increasing amount of time the calcium channel spends in the open state

61
Q

Adrenergic regulation of LTCC activity:
Increases/decreases the amount of calcium induced calcium release?

A

Increases

62
Q

What is rad?

A

A small Ras-lilke G protein which is a known inhibitor of voltage-gated calcium channels

63
Q

The interaction between Rad and what is essential for PKA regulation of Cav1.2 activity?

A

Interaction between rad and beta-2B is essential for PKA regulation of Cav1.2 activity

64
Q

Function of SERCA2A

A

Removal of calcium at the beat by pumping calcium from cytosol back into lumen of SR

65
Q

What regulates SERCA2A?

A

Nitric oxide

66
Q

How does phospholamban inhibit SERCA activity?

A

It reduces its affinity for Ca

CVDM (16 decks)

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