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My LSS- CVS > CVS 6: Blood vessel order > Flashcards

CVS 6: Blood vessel order Flashcards

1
Q

What are the three layers of blood vessels?

A
  1. Tunica Adventitia
  2. Tunica Media
  3. Tunica Intima
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2
Q

What is found in the tunica adventitia and what is its function?

A

The EXTERNAL Layer

  • contains fibrous tissue, elastin and collagen
  • helps keep shape of the blood vessel
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3
Q

What is the tunica media made of and what is its function?

A
  • Predominantly smooth muscle

- can contract or dilate based on the type of stimulus

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4
Q

What is the tunica intima made of and what is its function?

A
  • Vascular endothelium has an elastic basal lamina

- The exchange surface

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5
Q

What is the vascular endothelium?

A

A single cell layer that acs as the BLOOD-VESSEL interface

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6
Q

Give the five functions of vascular endothelium

A
  1. VASCULAR TONE- secretes and metabolises vasoactive substances (which cause vasodilation/constriction)
  2. THROMBOSTASIS- secretes anti-coagulants, prevents clotting and molecules adhering to vessel walls
  3. ABSORPTION + SECRETION
  4. BARRIER- prevents entry of pathogens and prevents atheroma formation
  5. GROWTH- mediates cell proliferation
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7
Q

What do endothelial cells contain to detect increased blood flow?

A

Mechanoreceptors

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8
Q

Name the two types of vasodilators and briefly summarise how they work.

A
  1. Nitric oxide- inhibits platelet aggregation

2. PG12 (prostacyclin)- cardioprotective molecule which also inhibits platelet aggregation

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9
Q

Name three vasoconstrictors and briefly summarise how they work.

A
  1. TXA2 (thromboxane)- produced in endothelial cells and platelets, activates other platelets–> aggregation
  2. ET-1 (endothelia 1)
  3. Angiotensin II (ANG II)
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10
Q

What controls vascular tone?

A

Balance between vasoconstriction and vasodilation

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11
Q

What is special about endothelin-1

A

Can cause vasoconstriction and vasodilation because it has different receptors on different tissues

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12
Q

What stimulates NO production and how?

A

Acetylcholine

  • It binds to the G protein coupled receptor
  • activates Phospholipase C
  • PLC converts PIP2=> IP3 and DAG
  • IP3 moves to the ER and causes Ca2+ efflux
  • A rise in IC Ca2+ up regulates endothelial nitric oxide synthase (eNOS)
  • eNOS catalyses formation of NO
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13
Q

Which reaction does eNOS catalyse?

A

L-arginine + O2==> L-citrulline + NO

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14
Q

How does NO work?

A
  • NO exits the endothelial cell and moves to the smooth muscle
  • NO in smooth muscle up-regulates Guanylyl cyclase which converts GTP to CGMP
  • cGMP up regulates Protein Kinase G
  • PKG activates potassium channels
  • membrane hyperpolarises
  • Relaxation of smooth muscle
  • Vessel dilates
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15
Q

What stimulates endothelial NO?

A

Shear stress (the force of blood going across the endothelial cells)

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16
Q

What acts as a NO donor?

A

SNP (Sodium nitroprusside)- we don’t rely on endothelial cells to produce NO. Endothelium is bypassed
Used to control high bp

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17
Q

What is used to convert phospholipids into Arachidonic acid?

A

Phospholipase A2

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18
Q

What is Arachidonic acid converted to? and using which enzyme?

A

Prostaglandin H2 (PGH2) by the COX enzymes (cyclooxygenase)- COX1 and COX2

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19
Q

Where is COX 1 found and what do an elevated levels of COX2 indicate?

A

COX1- expressed on all cells

COX2- unregulated when your body has inflammatory problems

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20
Q

What does PGH2 become and name the enzymes used…

A

PGH2==>

  1. Prostacyclin (PGI2)
    • Prostacyclin synthase
  2. Thromboxane A2 (TXA2)
    • Thromboxane synthase
  3. Other produces (PGD2, PGE2 and PGF2)
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21
Q

What is the function of some of the other products produced from PGH2?

A

Involved in the health of the epithelia and the GI tract

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22
Q

What other product might Arachidonic acid be converted to and which enzyme does this pathway use?

A

Leukotrines

Lipooxygenase enzyme cascade

23
Q

Give an example of a leukotrine and its effect in the body

A

LTD4- bronchoconstriction

LTD4 is associated with asthma

24
Q

Other than phospholipids what molecule can be used to form arachidonic acid? Which enzyme is used in this process?

A

DAG using DAG lipase

25
Where is prostacyclin produced and what is it produced from?
Produced in endothelial cells from arachidonic acid
26
What does prostacyclin bind to once it is produced in endothelial cells? What is the effect of this binding?
- Binds to IP receptor on smooth muscle. - Activates adenylate cyclase which converts ATP to cAMP - cAMP up regulates PKA which causes relaxation of smooth muscle=> vasodilation
27
What is the other effect of prostacyclin apart from vasodilation? How does this happen?
- Has anti-platelet aggregation properties | - Has to be secreted into the blood
28
Which two receptors can Thromboxane bind to?
Alpha- Platelets | Beta- Vascular smooth muscle cells
29
How does Thromboxane bring about vasoconstriction?
- TXA2 diffuses through the basement membrane - TXA2 binds to the TPB on VSMCs. - Activates PLC - PLC converts PIP2 into IP3 - IP3 triggers Ca2+ influx from EC space and SER - Ca2+ upregulates myosin light chain kinase which causes VSMC to contract - vasoconstriction
30
How does Thromboxane A2 bring about platelet aggregation?
- TXA2 binds to TPa receptors on platelets - Platelets become active and produce more TXA2 - Positive feedback response - Platelets aggregate
31
How and where is endothelia-1 produced?
- In the nucleus of endothelial cells - Endothelin-1 is produce from its zymogen (inactive precursor) by Endothelin Converting Enzyme (which is embedded in the membrane)
32
What happens to Endothelin-1 once it has been produced in the endothelial cells?
- Endothelin-1 binds to the ETA and ETB receptors on VSMCs - Receptors activate PLC which converts PIP2 to IP3 - IP3 triggers Ca2+ influx - This causes the cell to contact ==> Vasoconstriction
33
What is the alternative to Endothelin-1 binding to ETA and ETB on VSMCs?
- ET-1 could bind to ETB receptor on the endothelial cell - triggers eNOS - eNOS increases NO production - NO diffuses to VSMC - Cell relaxes and vessel dilates
34
What are the antagonists of ET-1 production?
- Prostacyclin - Nitric oxide - ANP - Heparin - HGF - EGF
35
What are the agonists of ET-1 production?
- Adrenaline - ADH - Ang II - IL-2
36
What is the precursor for angiotensin II? and where is it produced?
Angiotensinogen | Liver
37
What converts Angiotensinogen to Angiotensin I? Where is this enzyme produced and under what conditions is it produced?
1. Renin 2. Produced in the kidneys 3. Produced in response to Low blood pressure if renal perfusion decreases
38
What is Angiotensin I converted to and which enzyme does this? Where is this enzyme found?
1. Angiotensin II 2. Angiotensin Converting Enzyme (ACE) 3. Vascular endothelium
39
What are the two overall effects of Angiotensin II secretion?
1. Increased water retention | 2. Increase in vascular resistance
40
How is the increased water retention brought about by Angiotensin II?
- stimulates ADH secretion - Increases aldosterone production - Increases Sodium reabsorption
41
How is the increase in vascular resistance brought about?
- Increased sympathetic activity | - Arteriolar vasoconstriction
42
What is the effect of increasing vascular resistance and water retention?
Increases blood pressure
43
Describe how angiotensinogen is produced from angiotensin and then goes on to affecting arterioles
- Renin cleaves angiotensinogen to Ang I - ACE, expressed on endothelial cells in renal/ pulmonary circulation cleaves Ang I to Ang II - Ang II diffuses across the endothelium - Ang II binds to AT1 receptor on VSMC - Activates PLC which converts PIP2 to IP3 - IP3 triggers Ca2+ influx - Ca2+ up regulates MLCK - increases cross-bridging - Cell contracts and you get vasoconstriction
44
What other effect does ACE have?
ACE breaks down bradykinin | - NO-mediated vasodilation is reduced
45
What are the three ways of increasing the diameter of blood vessels and what sort of mechanisms do the use?
1. Stimulating production of NO (endothelium-dependent) 2. Donating Nitric Oxide (endothelium- independent) 3. Enhancing the effects of the NO that's already there (stopping its degradation)
46
Which enzyme does Viagra inhibit? Which reaction does this enzyme catalyse?
1. Phosphodiesterase 2. Involved in converting cGMP to GMP which is metabolically inactive 3. cGMP needed for vasodilation so viagra prevents cGMP inactivation
47
Which enzyme does aspirin affect?
Irreversible inhibition of the COX enzymes - COX1- inactivation - COX2- switches its function to generate protective lipids
48
What do non-specific NSAIDs cause?
reversible inhibition of COX enzymes
49
What is the consequence of Aspirin inhibiting the COX enzymes?
- Reduce conversion of Arachidonic acid to PGH2 | - less prostacyclin and thromboxane
50
What is the consequence of using a low dose of aspirin on the body?
- Prostacyclin levels decrease and then remain high | - Thromboxane levels continue to fall
51
Why do prostacyclin levels remain high while thromboxane levels fall whilst on low dose aspirin?
- Thromboxane is mainly produced in the platelets. | - Platelets don't have nuclei so they can't generate more mRNA to produce new proteins to build the COX enzymes again
52
Why can you use drug which block VGCC without affecting the heart?
- The affinity of the channel blocker to the channel is related to the membrane potential of the target cell - smooth muscle cells have higher membrane potentials than cardiomyocytes
53
What are the effects of ACE inhibitors?
- inhibit the conversion of Ang I to Ang II - We inhibit the breakdown of Bradykinin - Decreasing Bradykinin breakdown stimulates vasodilation
54
What happens if the endothelium is dysfunctional?
- damages - parts of sub-endothelial layer (collagen) is exposed - causes platelets to adhere - Platelets stick and release thromboxane - stimulates platelet aggregation - platelet plug forms

My LSS- CVS (21 decks)

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