6. Blood Vessel Order, Function and Specilisation Flashcards

1
Q

What are the layers in a blood vessel?

A

Tunica adventitia, Tunica media, Tunica intima

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2
Q

Describe the Tunica adventitia

A

External layer containing blood vessels, fibrous tissue, elastin, collagen.
Helps keep the shape of the blood vessel

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3
Q

Describe the Tunica media

A

Predominantly smooth muscle cells, able to contract or dilate

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4
Q

Describe the Tunica intima

A

Predominantly vascular endothelium with elastic basal lamina.
Exchange surface

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5
Q

Define vascular endothelium

A

A single cell layer that acts as the blood-vessel interface

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6
Q

What are the functions of the vascular endothelium?

A

Vascular tone management - Secretes and metabolises vasoactive substances
Thrombostasis - secretes anticoagulants
Absorption + Secretion
Barrier - Prevents atherosclerosis formation
Growth - mediates cell proliferation

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7
Q

What is the main principle that allows blood vessels regulate its own pressure?

A

Shear stress

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8
Q

What type of receptor in the endothelial cells detect increased blood flow?

A

mechanoreceptors

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9
Q

List vasodilators

A

Nitric oxide
Prostacyclin (PGI2)
Endothelin 1 (ET-1)

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10
Q

List vasoconstrictors

A
Thromboxane A2 (TXA2)
Endothelin 1 (ET-1)
Angiontensin II (ANG II)
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11
Q

How is vascular tone controlled?

A

The balance between the forces causing vasoconstriction and vasodilation

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12
Q

What will NO bind too in the blood?

A

G protein coupled receptor

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13
Q

What does the G couple protein receptor activate?

A

Phospholipase C (PLC)

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14
Q

What does PLC convert PIP2 into?

A

IP3 and DAG

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15
Q

Where does IP3 move to after being produced?

A

Endoplasmic reticulum

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16
Q

What does IP3 stimulate?

A

Calcium efflux

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17
Q

What does the rise in intracellular calcium cause?

A

Up-regulates endothelial nitric oxide synthase (eNOS)

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18
Q

What is the function of eNOS?

A

Catalyses the reaction:

L-arginine + oxygen –> L-citrulline + NO

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19
Q

Where does NO produced in the endothelial cell move to?

A

Smooth muscle cell

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20
Q

What does NO in the smooth muscle cell do?

A

Upregulates the activity of Guanylyl Cyclase

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21
Q

What is the function of guanylyl cyclase?

A

Converts GTP to cGMP

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22
Q

What is the function of cGMP?

A

It upregulates Protein Kinase G

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23
Q

What is the function of protein kinase G?

A

Protein Kinase G causes the relaxation of smooth muscle; Vasodilation

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24
Q

What can also act as a stimulator upregulating NO?

A

Shear stress

Acetylcholine

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25
Q

What happens if there is no endothelium?

A

There is no change in vessel diameter

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26
Q

What molecule can be used to produce arachidonic acid?

A

Phospholipid catalysed by Phospholipase A2

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27
Q

What is arachidonic acid a precursor to?

A

Prostacyclin (PGI2)
Thromboxane A2 (TXA2)
Leukotrienes - LTD4

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28
Q

How is arachidonic acid converted to prostaglandin H2 (PGH2)?

A

By cyclooxygenase enzymes (COX enzymes)

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29
Q

What cyclooxygenase enzyme is expressed in all cells?

A

COX 1

30
Q

What can prostaglandin H2 become?

A
Prostacyclin (PCI2) with prostacyclin synthase
Thromboxane A2 (TXA2) with thromboxane synthase
31
Q

What does LTD 4 cause?

A

Bronchoconstriction

32
Q

How is arachidonic acid converted to leukotrienes?

A

Lipoxygenase enzyme cascade

33
Q

What is function of prostacyclin?

A

Vasodilation, inhibits the formation of atheromatous plaque and stops the aggregation of platelets.

Thromboxane works against these all - typically bad for the cardiovascular system
Prostacyclin has cardioprotective properties

34
Q

What DAG be converted to?

A

Archidonic acid by DAG lipase

35
Q

Where is prostacyclin produced?

A

Endothelial cells

36
Q

Where does prostacyclin bind to?

A

It binds to IP receptors which is coupled with adenylate cyclase on smooth muscle cells

37
Q

What does the IP receptor coupled with an adenylate cyclase do?

A

Converts ATP to cAMP

38
Q

What does cAMP do?

A

Upregulates Protein Kinase A

39
Q

What is function of Protein Kinase A?

A

Causes the relaxation of smooth muscle; Vasodilation

40
Q

What can thromboxane bind to?

A

Alpha receptors - platelets

Beta receptors - Vascular smooth muscle cells

41
Q

What is the beta receptor on smooth muscle cells coupled with?

A

Phospholipase C

42
Q

What happens when thromboxane binds to alpha receptors?

A

It activates platelets causing the production of more thromboxane. Stimulates aggregation

43
Q

How is endothelin-1 produced?

A

An endothelin precursor in the nucleus is cleaved by endothelin converting enzyme

44
Q

Where does endothelin-1 bind to?

A

It binds to alpha and beta receptors on smooth muscle

45
Q

What are both alpha and beta receptors bound to on smooth muscle cells?

A

PLC - converting PIP2 to IP3 and DAG. These receptors are found on smooth muscle and cause contraction

46
Q

What happens when endothelin-1 binds to a beta receptor on the endothelial cell?

A

It triggers the activation of eNOS causing relaxation

47
Q

What are the antagonists which inhibits the production of endothelin-1 prescursor?

A
o Prostacyclin
o Nitric Oxide
o ANP (atrial natriuretic peptide)
o Heparin
o HGF (hepatocyte growth factor)
o EGF (epidermal growth factor)
48
Q

What are the antagonists which stimulate the production of endothelin-1

A

o Adrenaline
o Vasopressin
o Angiotensin II
o Interleukin-1

49
Q

What is the function of angiotensin II?

A

o Stimulates ADH secretion
o Increases aldosterone production
o Increases sodium reabsosorption
ALL THREE OF THESE CAUSE INCREASED WATER RETENTION

o Increased sympathetic activity
o Arteriolar vasoconstriction
BOTH CAUSE AN INCREASE IN VASCULAR RESISTANCE

50
Q

What does an increase in vascular resistance and an increase in water retention lead to?

A

Increase in blood pressure

51
Q

What is the precursor for angiotensin II?

A

Angiotensinogen

52
Q

What is secreted in response to low blood pressure?

A

Renin in the kidney

53
Q

What is the function of renin?

A

It converts angiotensinogen to angiotensin I

54
Q

What converts angiotensin I to angiotensin II?

A

Angiotensin Converting Enzyme (ACE)

55
Q

What does activation of PLC on smooth muscle cause?

A

Contraction

56
Q

Why does IP3 production cause contraction in smooth muscle cells?

A

The increase in calcium increases the amount of cross-bridge cycling that takes place

57
Q

What does angiotensin II bind to?

A

Antiotensin receptor which activates PLC

58
Q

What is the overall effect of angiontensin II

A

Increases blood pressure

59
Q

What breaks down bradykinin?

A

ACE

60
Q

What is the function of bradykinin?

A

Stimulates vasodilation

61
Q

What can bradykinin bind to?

A

Bradykinin receptor-1 on endothelial cells which activates PLC which converts PIP2 to IP3 which upregulates NO production

62
Q

How can increase the amount of NO available vasodilation?

A

1) Stimulating the production of nitric oxide - Endothelium dependent
2) Donating nitric oxide - Endothelium independent

63
Q

What is a nitric oxide donor?

A

SNP (sodium nitroprusside)

64
Q

What activates guanylyl cyclase?

A

Endogenous and exogenous NO

65
Q

How does viagra work?

A

It inhibits phosphodiesterase (PDES) which prevents cGMP to being converted to GMP

66
Q

What does aspirin cause?

A

Irreversible inhibition of the COX enzymes

67
Q

What effect does aspirin have on COX 1 and COX 2?

A

COX 1 - Inactivation

COX 2 - Switches its function

68
Q

What is the effect of low dose aspirin?

A

It will slightly decrease the levels of prostacyclin but cause thromboxane levels to continually fall.

69
Q

What happens when you inhibit ACE?

A

Angiotensin II is not produced and bradykinin is not broken down hence causing vasodilation.

70
Q

How does a platelet plug form?

A

When the endothelium is damaged platlets adhere to exposed collagen and release thromboxane. This causes the aggregation of platlets forming a platelet plug

71
Q

List some antihypertensive medication

A

Angiotensin receptor blockers
ACE inhibitors
Calcium channel blockers