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Year 1: Cardiovascular System > 6. Blood Vessel Order, Function and Specilisation > Flashcards

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
What happens if there is no endothelium?
There is no change in vessel diameter
26
What molecule can be used to produce arachidonic acid?
Phospholipid catalysed by Phospholipase A2
27
What is arachidonic acid a precursor to?
Prostacyclin (PGI2) Thromboxane A2 (TXA2) Leukotrienes - LTD4
28
How is arachidonic acid converted to prostaglandin H2 (PGH2)?
By cyclooxygenase enzymes (COX enzymes)
29
What cyclooxygenase enzyme is expressed in all cells?
COX 1
30
What can prostaglandin H2 become?
``` Prostacyclin (PCI2) with prostacyclin synthase Thromboxane A2 (TXA2) with thromboxane synthase ```
31
What does LTD 4 cause?
Bronchoconstriction
32
How is arachidonic acid converted to leukotrienes?
Lipoxygenase enzyme cascade
33
What is function of prostacyclin?
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
What DAG be converted to?
Archidonic acid by DAG lipase
35
Where is prostacyclin produced?
Endothelial cells
36
Where does prostacyclin bind to?
It binds to IP receptors which is coupled with adenylate cyclase on smooth muscle cells
37
What does the IP receptor coupled with an adenylate cyclase do?
Converts ATP to cAMP
38
What does cAMP do?
Upregulates Protein Kinase A
39
What is function of Protein Kinase A?
Causes the relaxation of smooth muscle; Vasodilation
40
What can thromboxane bind to?
Alpha receptors - platelets | Beta receptors - Vascular smooth muscle cells
41
What is the beta receptor on smooth muscle cells coupled with?
Phospholipase C
42
What happens when thromboxane binds to alpha receptors?
It activates platelets causing the production of more thromboxane. Stimulates aggregation
43
How is endothelin-1 produced?
An endothelin precursor in the nucleus is cleaved by endothelin converting enzyme
44
Where does endothelin-1 bind to?
It binds to alpha and beta receptors on smooth muscle
45
What are both alpha and beta receptors bound to on smooth muscle cells?
PLC - converting PIP2 to IP3 and DAG. These receptors are found on smooth muscle and cause contraction
46
What happens when endothelin-1 binds to a beta receptor on the endothelial cell?
It triggers the activation of eNOS causing relaxation
47
What are the antagonists which inhibits the production of endothelin-1 prescursor?
``` o Prostacyclin o Nitric Oxide o ANP (atrial natriuretic peptide) o Heparin o HGF (hepatocyte growth factor) o EGF (epidermal growth factor) ```
48
What are the antagonists which stimulate the production of endothelin-1
o Adrenaline o Vasopressin o Angiotensin II o Interleukin-1
49
What is the function of angiotensin II?
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
What does an increase in vascular resistance and an increase in water retention lead to?
Increase in blood pressure
51
What is the precursor for angiotensin II?
Angiotensinogen
52
What is secreted in response to low blood pressure?
Renin in the kidney
53
What is the function of renin?
It converts angiotensinogen to angiotensin I
54
What converts angiotensin I to angiotensin II?
Angiotensin Converting Enzyme (ACE)
55
What does activation of PLC on smooth muscle cause?
Contraction
56
Why does IP3 production cause contraction in smooth muscle cells?
The increase in calcium increases the amount of cross-bridge cycling that takes place
57
What does angiotensin II bind to?
Antiotensin receptor which activates PLC
58
What is the overall effect of angiontensin II
Increases blood pressure
59
What breaks down bradykinin?
ACE
60
What is the function of bradykinin?
Stimulates vasodilation
61
What can bradykinin bind to?
Bradykinin receptor-1 on endothelial cells which activates PLC which converts PIP2 to IP3 which upregulates NO production
62
How can increase the amount of NO available vasodilation?
1) Stimulating the production of nitric oxide - Endothelium dependent 2) Donating nitric oxide - Endothelium independent
63
What is a nitric oxide donor?
SNP (sodium nitroprusside)
64
What activates guanylyl cyclase?
Endogenous and exogenous NO
65
How does viagra work?
It inhibits phosphodiesterase (PDES) which prevents cGMP to being converted to GMP
66
What does aspirin cause?
Irreversible inhibition of the COX enzymes
67
What effect does aspirin have on COX 1 and COX 2?
COX 1 - Inactivation | COX 2 - Switches its function
68
What is the effect of low dose aspirin?
It will slightly decrease the levels of prostacyclin but cause thromboxane levels to continually fall.
69
What happens when you inhibit ACE?
Angiotensin II is not produced and bradykinin is not broken down hence causing vasodilation.
70
How does a platelet plug form?
When the endothelium is damaged platlets adhere to exposed collagen and release thromboxane. This causes the aggregation of platlets forming a platelet plug
71
List some antihypertensive medication
Angiotensin receptor blockers ACE inhibitors Calcium channel blockers

Year 1: Cardiovascular System (21 decks)

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