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Cardiovascular System Module > Lecture 14 > Flashcards

Lecture 14 Flashcards

1
Q

What happens when the endothelium is removed?

A

Acetylcholine results in contraction

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2
Q

What happens when endothelium is present?

A

Acetylcholine results in relaxation

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3
Q

What was discovered when the epithelium was present?

A

EDRF - endothelium derived relaxing factor

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4
Q

What was the EDRF identified as?

A

The gas nitric oxide

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5
Q

Why did Robert Furchgott, Louis Ignarro and Ferid Murad win the normal prize in 1998?

A

For their discoveries concerning nitric oxide as a signalling molecule in the cardiovascular system

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6
Q

What does NO generate?

A

Smooth muscle relaxation via stimulation of cGMP production

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7
Q

How is NO broken down?

A

It is rapidly broken down by free radicals (O2-) and by haemoglobin

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8
Q

What is the NO signalling pathway synthesised from?

A

L-arginine by eNOS (endothelial nitric oxide synthase)

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9
Q

What does NO toncially control?

A

Vascular resistance

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10
Q

How can you inhibit eNOS?

A

With L-NMMA which Inhibits blood flow by 50%

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11
Q

What is the inhibition of eNOS reversed by?

A

L-arginine

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12
Q

How often is NO released?

A

It is released continuously to control blood flow

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13
Q

What is the most important control of NO release?

A

SHEAR STRESS is the signal, not flow

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14
Q

What does an increase in NO synthesis increase?

A

It is increases with blood viscosity at a constant flow rate

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15
Q

What does the degradation of glycocalyx =

A

Reduction in flow-induced NO production

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16
Q

What is the stress signal transduced by?

A

Endothelial glycocalyx (integrins)

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17
Q

What do integrins activate?

A

Phosphatidyl inositol 3 kinase

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18
Q

What is the mechanisms for shear stress-induced NO production?

A

Stress signal is induced by endothelial glycocalyx,
Which actuates phosphatidyl inositol 3 kinase
Which phosphorylates protein kinase B
Which phosphorylates eNOS
And increase eNOS activity

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19
Q

What does NO couples flow in?

A

Arterioles and conduit arteries

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20
Q

What is metabolic hyperaemia?

A

Local control of blood flow

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21
Q

What is the pathway for NO flow in arterioles and conduit arteries?

A

Vasodilation of arterioles,
Increase flow rate in upstream conduit artery,
Increase shear stress
Increase NO release

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22
Q

What is another mechanism of endothelium-dependent relaxation?

A

Acetylcholine causes arterial relaxation and hyperpolarisation of smooth muscle cells

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23
Q

What is another way for endothelium-dependent relaxation?

A

Inhibition of eNOS and PGI2 production which blocks later relaxation phase

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24
Q

What is the early phase of hyperpolarisation and relaxation mediated by?

A

Endothelium dependent hyperpolarising factor (EDHF)

25
Q

What causes hyperpolarisation of the endothelial cell?

A

An agonist

26
Q

How can hyperpolarisation spread through the cell?

A

Via gap junctions

27
Q

What are candidate EDHFs?

A

K+, EET, hydrogen peroxide, c-natriuretic peptide

28
Q

What are the agonists that cause hyperpolarisation through the cell?

A

Thrombin, bradykinin, acetylcholine

29
Q

What are some examples of endothelium derived vasoactive substances?

A

Nitric oxide, EDHF, prostacyclin (PGI2), endothelin

30
Q

What does the EDHF factor do?

A

Causes vasodilation in small vessels, especially arterioles

31
Q

What is prostacyclin derived from?

A

Arachidonic acid

32
Q

What does prostacyclin do?

A

Vasodilation and prevents platelet adhesion to endothelial cells

33
Q

Describe endothelin?

A

It’s a peptide, contributes to vasoconstriction and has a small contribution to basal vascular tone

34
Q

Do NO, EDHF and PGI2 vary?

A

They vary between arterioles of different diameters and from different vascular beds

35
Q

Where is NO found in disease?

A

In essential hypertension, secondary hypertension, diabetes 1,2 and atheroma and dyslipidemia

36
Q

What is the role of NO in essential hypertension?

A

Abnormal production of NO implicated

37
Q

What is secondary hypertension?

A

Increased release of asymmetric dimethylarginine from damaged kidney

38
Q

What is the role of NO in diabetes 1 and 2?

A

Associated with a decreased NO production and decreased NO induced relaxation. Evidence of decreases insulin-mediated NO production

39
Q

What is the role of NO in septic shock?

A

Increase stimulation of iNOS production in macrophages and endothelial cells = massive vasodilation and increase in capillary permeability

40
Q

What does iNSO mean?

A

Inducible NOS

41
Q

What does septic shock result in?

A

Fall in blood pressure often fatal

42
Q

What could reverse hypotension?

A

L-NMMA treatment

43
Q

Describe the mechanism involved in NO formation and vasodilation?

A

Increases in ca2+ in endothelial cells induced by stimuli such as shear stress, blood flow and binding of agonists leads to formation of a ca2+ calmodulin complex which activates NO

44
Q

What is eNOS response for?

A

Most of the vascular NO production

45
Q

What happens to eNOS in a pathological state?

A

Becomes a potential ROS (reactive oxygen species) generator due to various oxidative stress

46
Q

What are the 3 different signalling pathways that regulate vascular tone?

A

Ca2+ signalling pathway, NO-cGMP, vascular signalling pathway

47
Q

What is vascular remodelling?

A

Alteration in radius of blood vessel and alteration in wall thickness of blood vessel

48
Q

What does outward remodelling result in?

A

Increased diameter

49
Q

What does inward remodelling result in?

A

Decreased diameter

50
Q

When does remodelling take place?

A

Physiological conditions, high altitude, endurance training and pathophysiological conditions

51
Q

Examples of physiological conditions?

A

Ageing, pregnancy

52
Q

High altitude examples?

A

Acute hypoxia, cerebral and pulmonary oedema, prolonged hypoxia

53
Q

What does endurance training change?

A

Conduit vessels have larger diameter, increase in number/density of arterioles (remodelling of capillaries driven by increase shear stress), capillary angiogenesis (VEGF) and increased mitochondria in muscle cells

54
Q

What VEGF?

A

Vascular endothelial growth factor

55
Q

Why could there be remodelling of vascular smooth muscle cells?

A

Responses to prolonged stimulation or pathophysiological insults

56
Q

What is the shift from a contractile to synthetic phenotype in smooth muscle cells associated with?

A

Reduction in myosin expression and molecular and functional alterations in ca2+ signalling

57
Q

What are examples of molecular and functional alterations in ca2+ signalling?

A

A move from L type to T type channel ca2+ entry, increasing involvement of TRP proteins in ca2+ cycling and switch in caMK11 isoforms

58
Q

What happens to vascular smooth muscle in response to injury?

A

It undergoes a phenotypic switch, a process that contributes to pathophysiological vascular wall remodelling

Cardiovascular System Module (18 decks)

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