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LSS Cardiovascular System > 7 Blood Vessel Order, Function and Specialisation > Flashcards

7 Blood Vessel Order, Function and Specialisation Flashcards

1
Q

Q: What are the 3 layers of blood vessels? Describe what each layer contains and role.

A

A: Tunica adventitia

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

Tunica media

  • Predominantly smooth muscle cells
  • able to contract or dilate depending on the type of stimulus

Tunica intima

  • Predominantly vascular endothelium has the elastic basal lamina as well
  • this is the exchange surface
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2
Q

Q: What is the vascular endothelium? 5 role?

A

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

  • vascular tone:
  • thrombostasis:
  • absorption/secretion: active/passive transport via diffusion/channels
  • barrier
  • growth/repair: mediates cell proliferation
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3
Q

Q: Vascular endothelium role. How does it control vascular tone? allowing? (2) acts as? Explain.

A

A: secretes and metabolises vasoactive substances – this can cause vasoconstriction or vasodilation (kind of like a local paracrine gland)

= blood vessels locally sense and locally react and change because of endothelium

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4
Q

Q: Vascular endothelium role. Thrombostasis?

A

A: prevents clot formation or molecules adhering to wall (secretes anti-coagulant substances)

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5
Q

Q: Vascular endothelium role. How does it act as a barrier? (2)

A

A: prevents atheroma (fatty material which forms deposits in the arteries) development and impedes pathogens

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6
Q

Q: What are the 5 key mediators of vasoconstriction and dilation?

which inhibits platelet _?

A

A: VASODILATORS

  • Nitric Oxide
  • PGI2 (prostacyclin) also inhibits platelet aggregation

VASOCONSTRICTORS

  • TXA2 (thromboxane)
  • ET-1 (endothelin 1)
  • Angiotensin II (ANG II)
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7
Q

Q: What causes hypertension in terms of vascular tone? Treated hypertension?

A

A: HT: vasoconstriction aspect is more active <= trying to close off vessel

tHT: given drugs that allow the balancing out of it (shift in other direction)

  • ignore vasoconstricting factors OR
  • increase vasodilating ones
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8
Q

Q: What 2 methods allow the assessment of endothelial function? Clinical practice?

A

A: laser doppler flowmetry

flow-mediated dilation

not used clinically as not accurate enough and difficult to interpret (lots of variability)

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9
Q

Q: What is laser doppler flowmetry? Describe (3).

A

A: method of assessing endothelial function

  1. Intact endothelium with regular delivery of ACh -> blood flow increased more and more with each delivery= blood vessels get wider
  2. No endothelium with delivery of ACh= no response
  3. Exogenous NO-donor = vasodilator -> creates similar graph to 1 (acts as control test)
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10
Q

Q: What is flow mediated dilation? (5)

A

A: method of assessing endothelial function

measure blood flow through brachial artery and can stimulate an increase in blood flow

leads to increase in local shear stress= force of blood going across the endothelial cells

stimulator - it can upregulate endothelial NO

get vasodilation/ artery widens

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11
Q

Q: How is arachidonic acid made? What is it is? What happens to it?

A

A: formed from phospholipid from lipid bilayer via E: phospholipase A2

precursor to many molecules

converted to Prostaglandin H2 (PGH2) by the COX1 and 2 enzymes (COX = cyclooxygenase)

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12
Q

Q: What is PGH2? What can it become? (3) (include actions of molecules produced)

A

A: molecule made from arachidonic acid (by COX 1 and 2 enzymes-cyclooxygenase)

E: Thromboxane Synthase -> thromboxane A2 (TXA2)

  • vasoconstricter
  • pro-atherogenic
  • pro-platelet

E: prostacyclin synthase -> prostacyclin

  • vasodilator
  • anti-atherogenic
  • anti-platelet

PGD2, PGE2, PGF2
-all are typically involved in pain, fever and inflammation

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13
Q

Q: How and where is nitric oxide produced (NO)? (6) 2 other stimuli?

A

A: 1. stimulus: ACh binding to G protein associated receptor that has phospholipase C attached

  1. PLC migrates along membrane until it reaches PIP2 (which is embedded in the membrane)
  2. PLC converts PIP2 to IP3 and DAG
  3. IP3 triggers Ca2+ influx from ER
  4. rise in intracellular calcium concentration upregulates endothelial nitric oxide synthase (eNOS)
  5. eNOS catalyses the following conversion:
    L-arginine + Oxygen -> L-citrulline + NO

eNOS = also stimulated by:

  • sheer stress of blood flow
  • NO can be delivered (attached to inert molecule) and taken to target tissue-> where it dissociates

made in the endothelial cells

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14
Q

Q: What happens to nitrous oxide once it is made? (7) Effect on blood vessel?

A

A: made in the endothelial cells

  1. exits and enters vascular smooth muscle via diffusion
  2. enzyme guanylase cyclase is upregulated as a result
  3. GC converts GTP to cGMP= part of smooth muscle cell secondary messenger system
  4. cGMP upregulates protein kinase G
  5. PKG activates K+ channels
  6. membrane hyperpolarises
  7. cell relaxes-> vessel dilation
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15
Q

Q: How and where is prostacyclin made? (4-making precursor, 1 alternative, 2)

A

A: endothelial cells

PGI2= prostacyclin

(1. stimulus: ACh binding to G protein associated receptor that has phospholipase C attached
2. PLC migrates along membrane until it reaches PIP2 (which is embedded in the membrane)
3. PLC converts PIP2 to IP3 and DAG
4. DAG-> via E: DAG ligase-> arachindonic acid)

ORRR

comes from phospholipid -> E: phospholiase A2

  1. arachnadonic acid -> converted to Prostaglandin H2 (PGH2) by the COX1 and 2 enzymes (COX = cyclooxygenase)
  2. PGH2 -> PGI2 by E: prostacylcin synthase
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16
Q

Q: What happens to prostacyclin once it’s made? Effect on blood vessel? What else does it affect?

A

A: made in endothelial cells

  1. PGI2 diffuses out of endothelial cells and binds to AT2 receptor on vascular smooth muscle cells
  2. upregulation of adenylase cyclase (attached to receptor)
  3. AC converts ATP-> cAMP
  4. cAMP inhibits myosin light chain kinase (MLCK)
  5. reduction of cross bridge cycling
  6. cell relaxes and blood vessel vasodilates

also secreted into the blood where it has anti-platelet aggregation properties

17
Q

Q: How and where is thromboxane A2 produced? (4-making precursor, 1 alternative, 2)

A

A: endothelial cells

TXA2

(1. stimulus: ACh binding to G protein associated receptor that has phospholipase C attached
2. PLC migrates along membrane until it reaches PIP2 (which is embedded in the membrane)
3. PLC converts PIP2 to IP3 and DAG
4. DAG-> via E: DAG ligase-> arachindonic acid)

ORRR

comes from phospholipid -> E: phospholiase A2

  1. arachnadonic acid -> converted to Prostaglandin H2 (PGH2) by the COX1 and 2 enzymes (COX = cyclooxygenase)
  2. PGH2 -> TXA2 by thromboxane synthase
18
Q

Q: How does TXA2 act when it’s made? (6,5) How does it affect blood vessels?

A

A: thromboxane A2 = made in epithelial cells

(can diffuse through both the apical and basal membrane)

  1. diffuses through basal membrane
  2. binds to TP beta receptor on the vascular smooth muscle cell (which is associated with phospholipase C)
  3. PLC converts PIP2 into IP3 in smooth muscle cell
  4. IP3 triggers Ca2+ influx into cell from extracellular space and sER
  5. Ca2+ upregulates myosin light chain kinase MLCK= increased amount of cross bridge cycling
  6. VSMC contracts and vessel constricts
  7. diffuses through apical membrane
  8. binds to TP-alpha on quiescent platelets
  9. platelets are activated and produce more TP-alpha
  10. more platelets activated-> positive feedback (continues until stimulus is removed)
  11. platelets aggregate
19
Q

Q: How is angiotensin II made? (4) Where?

A

A: in blood

  1. from liver: precursor= angiotensinogen made (not metabolically active/ zymogen)
  2. in presence of renin (made in kidney in response to low blood flow/hypoxia) will become angiotensin I (by cleavage process)
  3. angiotensin I is exposed to endothelial enzymes- either in pulmonary or renal circulation-> both express ACE
  4. angiotensin I -> II (cleavage process)
20
Q

Q: What are the 5 roles of angiotensin II? 2 overarching results? Overall effect?

A

A: -Stimulates ADH/vasopressin secretion from (post) pituitary gland

  • Increases aldosterone production= increases reabsorption in kidneys-> changes osmotic fluid balance
  • Increases tubular sodium reabsosorption (local receptors)

ALL THREE OF THESE CAUSE INCREASED WATER RETENTION

  • Increased sympathetic activity / sympathoexcitation -> leads to vasoconstriction
  • Arteriolar vasoconstriction (binds to receptors on VSMC -> shortening of cells)

BOTH CAUSE AN INCREASE IN VASCULAR RESISTANCE

overall= increased blood pressure

21
Q

Q: What happens to angiotensin II when it is made? (6) Effect on blood vessel?

A

A: 1. diffusion from blood across endothelium

  1. binds to AT1 receptor on vascular smooth muscle cells (associated with PLC)
  2. PLC migrates along membrane and converts PIP2 into IP3
  3. IP3 triggers calcium influx
  4. Ca2+ upregulates myosin light chain kinase MLCK= increased amount of cross bridge cycling
  5. VSMC contracts and vessel constricts
22
Q

Q: How in endothelin 1 made? (2) Where?

A

A: endothelial cells

  1. endothelial cell nucleus produces Big Endothelin 1 (precursor)
  2. endothelin converting enzyme (on inner cell membrane) converts zymogen to ET-1 (active form)
23
Q

Q: How does ET-1 act once it’s produced? (6,4)

A

A: endothelin 1

  1. diffuses out of endothelial cell
  2. binds to ETalpha and ETbeta on vascular smooth muscle cell that are associated with PLC
  3. PLC migrates along membrane and converts PIP2 into IP3
  4. IP3 triggers calcium influx
  5. Ca2+ upregulates myosin light chain kinase MLCK= increased amount of cross bridge cycling
  6. VSMC contracts and vessel constricts

OR

  1. binds to ET beta receptor on endothelial cells
  2. causes upregulation of eNOS (endothelial nitric oxide synthase)
  3. eNOS catalyses the following conversion:
    L-arginine + Oxygen -> L-citrulline + NO => means you get more NO produced
  4. enters vascular smooth muscle via diffusion-> low intra [Ca2+] -> relaxation -> vasodilation
24
Q

Q: Which effect of endothelin 1 dominates? Generally?

A

A: depends on which receptors are more expressed- those on endothelial cell (ET beta) or VSMC (ET alpha and beta)

has a contracting effect/ vasoconstricting

25
Q

Q: What can effect the production of endothelin 1? (2) Examples (6,4).

A

A: antagonists- inhibit the production of the endothelin-1 precursor

Agonists which stimulate the production of endothelin-1

Antagonists

  • Prostacyclin/ PGI2
  • Nitric Oxide/ NO
  • ANP (atrial natriuretic peptide)
  • Heparin
  • HGf (hepatocyte growth factor)
  • EGf (epidermal growth factor)

Agonists

  • adrenaline
  • Vasopressin/ADH
  • Angiotensin II
  • Interleukin-1
26
Q

Q: What is viagra? Mechanism?

A

A: phosphodiesterase inhibitor

reduces break down of No 2nd messenger system

27
Q

Q: What’s the effect of medication with NO functional groups? Downside? Used to treat? Downside? explain.

A

A: nitric oxide

donates ‘ready to use’ NO -> allows vasodilation and lowering of bp

but NO has short half life-> so is short acting

mainly angina

  • can make you light headed and faint/ head aches
  • as blood vessels in brain start to get wider= compressing on brain
28
Q

Q: What happens when you block the flow of calcium into cells (VSMC)? Specificity? (3)

A

A: impedes cross bridge cycling which is Ca2+ dependant

-> lowers bp (can treat hypertension)

There needs to be a way to block certain calcium channels without affecting the calcium channels in the heart

It just so happens that the affinity of the channel blocker to the channel is related to the MEMBRANE POTENTIAL OF TARGET CELLS

Smooth muscle cells have a higher membrane potential (more positive) than cardiomyocytes

29
Q

Q: What’s the effect of ACE inhibitors and angiotensin II receptor blockers? (3) Overall effect? Used to treat?

A

A: by inhibiting ACE-> inhibit ANG II production (which is a vasoconstricter)

inhibiting ACE also reduces degradation of bradykinin in blood (which is a vasodilator)

blocking receptors-> stop them carrying out their effect as vasoconstricters

  • decrease bp/ vasodilation
  • hypertension
30
Q

Q: What is the extracellular concentration of Ca2+? Intracellular? Result? Reverse?

A

A: 2mmol/L (around 20000x)

100nmol/L

moves quickly into cells due to high gradient (no energy required)

would need energy, pumps, contransporters -> against concentration gradient

31
Q

Q: What is aspirin? what does it do? (2) 2 ways? Variation?

A

A: irreversible COX inhibitor= prevents formation of prostoglandins = platelets can’t recover, endothelial cells produce more enzymes

  1. aspirin acetylation of COX 1 inactivate the E
  2. aspirin acetylation switches its function (to generating protective lipids)

COX 2 specific inhibitors cause reversible inhibition of COX 2 isoforms only

32
Q

Q: Compare the expression of COX 1 and 2.

A

A: 1= constituately expressed (all the time)

2= during periods of high inflammation

33
Q

Q: Draw a graph of X= consecutive days of low dose aspirin by Y= proportion (%). 3 lines. Why is there a difference?

A

A: REFER

prostacyclin

thromboxane

thromboxane (higher dose aspirin)

(for a week)

low-dose aspirin blocks the synthesis of Thromboxane-A2 and not Prostacyclin -> because platelets are enucleated

34
Q

Q: What are NSAIDs? What can they do?

A

A: Non-steroidal anti-inflammatory drugs

cause reversible inhibition of COX enzymes

35
Q

Q: Explain why certain drugs give us (adverse) side effects. Variation?

A

A: -our body often uses the same biochemicals to regulate different processes
-but drugs aren’t tissue specific

AND receptor expression and distribution varies between tissues-> 2 taking taking same medication can have very different experiences

36
Q

Q: Fill in the table:

  1. nitric oxide (NO)
  2. prostacyclin (PGI2)
  3. thromboxane A2 (TXA2)
  4. endothelin 1 (ET1)
  5. angiotensin II (AG II)
  6. precursor (source)
  7. enzyme
  8. role of endothelial cell
  9. VSMC receptor
  10. VSMC second messenger
  11. effects on VSMC
  12. effects on platelets
A

A: REFER

37
Q

Q: Why does low-dose aspirin block the synthesis of Thromboxane-A2 and not Prostacyclin? Explain (3)

A

A: platelets are enucleated

Platelets have no nucleus to replace the COX enzymes that aspirin permanently disables.

New production relies on the production of new platelets.

Conversely, endothelial cells can generate new enzymes from their nucleus.

LSS Cardiovascular System (17 decks)

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