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CVS > CVS 6 - Blood vessel order, functions & specialisation of cells in the CVS > Flashcards

CVS 6 - Blood vessel order, functions & specialisation of cells in the CVS Flashcards

1
Q

What is the vascular endothelium?

A

Single cell layer that acts as the blood-vessel interface.

Has multitude of important functions.

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2
Q

What are the 5 key functions of the endothelium?

A
  • Vascular tone -> secretes and metabolises vasoactive substances (constriction/dilation)
  • Thrombostasis -> prevents clots forming or molecules adhering to vessel wall
  • Absorption & secretion -> Allows active/passive transport via diffusion/channels
  • Barrier -> prevent atheroma development and impedes pathogens
  • Growth -> mediates cell proliferation
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3
Q

How is endothelial function assessed?

A

By Laser Doppler flowmetry
Can compare change in blood flow with different administrations (like ACh) and also when endothelium is damaged/healthy to see difference.

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4
Q

What is arachidonic acid? Describe how it is produced.

A

Formed from phospholipids out of lipid bilayer with enzyme Phospholipase A2.
It is a precursor for a lot of things such as
Prostacyclin, Thromboxane A2 and prostaglandins typically involved in pain, fever, inflammation.

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5
Q

How are Thromboxane A2 and prostacyclin (PGI2) synthesised from arachidonic acid?

A

Arachidonic acid ————-> Prostaglandin H2 (PGH2)
Enzyme: COX1 + COX2
Prostaglandin H2 can then be converted to:
Thromboxane A2 (by Thromboxane Synthase)
Prostacyclin (by Prostacyclin Synthase)

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6
Q

What is the action of thromboxane A2 and prostacyclin?

A

Thromboxane A2: Vasoconstrictor (++)
Pro-platelet
Pro-atherogenic

Prostacyclin does the opposite even if they have the same precursor PGH2
Vasodilator (–)
Anti-platelet
Anti-atherogenic

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7
Q

What are the two main vasodilatory molecules? What other effect do they have?

A

Nitric Oxide
Prostacyclin
Inhibit the aggregation of platelets

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8
Q

What are the three main vasoconstricting molecules? Which of them has an effect on platelets?

A

Thromboxane A2 - activates platelets
Endothelin-1
Angiotensin II

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9
Q

What is special about endothelin-1?

A

Endothelin-1 can cause BOTH vasoconstriction AND vasodilation - it has different receptors on different tissues
However more potent vasocontrictor

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10
Q

Describe the synthesis of nitric oxide.

A

A substrate, ACh, that triggers NO production will bind to a Gq protein linked receptor and activate PLC. This migrates along membrane and sees PIP2:
PIP2 —-> IP3 + DAG
IP3 —-> triggers [Ca2+] release from SR
Increased [Ca2+] —> activates endothelial nitric oxide synthase (eNOS)
eNOS converts:
L-arginine + Oxygen —> L-citrulline + NO
(NO then diffuses into VSCM)

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11
Q

Describe the action of nitric oxide.

A

Nitric Oxide diffuses into cell and activates GUANYLYL CYCLASE (GC)—> transforms GTP to cGMP (this will be part of the cell secondary messenger system)—> activation of Protein Kinase G —> causes K influx –> RELAXATION

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12
Q

What is the precursor and source of NO?

A

Precursor: L-Arginine

Diet

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13
Q

What is the enzyme in NO synthesis?

A

eNOS

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14
Q

What is the role of the endothelial cell in NO synthesis and action?

A

Source of eNOS

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15
Q

What is the VSMC second messenger for NO?

A

GC

GC converts GTP to cGMP

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16
Q

What is the NO receptor on the VSMC?

A

There is no receptor. NO diffuses directly into cell and activates GC.

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17
Q

What role does acetylcholine play in blood vessels?

A

Acetylcholine UPREGULATES eNOS

This leads to steady vasodilation

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18
Q

What enzyme produces arachidonic acid from DAG?

A

DAG lipase

19
Q

What is the precursor of prostacyclin? How is it obtained in the endothelial cell?

A

Arachidonic acid.
Can be produced from DAG with DAG lipase (this is produced like for NO; bindin of ACh to endothelial cell activates PLC then PIP2 which is converted to DAG or IP3) or from phospholipid by phospholipase A2.

20
Q

Describe the mechanism of action of prostacyclin.

A

Prostacyclin binds to IP1 receptor on VSMC and activates AC —> increase in cAMP —> activate PKA —> inhibits MLCK –> reduces cross bridges cycling –> relaxation

21
Q

What is the role of the endothelial cell in PGI2 synthesis?

A

Major source of PGH2 (from which PGI2 is synthesised with prostacyclin synthase)

22
Q

What is prostacyclin’s receptor?

A

IP1

23
Q

What is prostacyclin’s VSMC second messenger?

A

AC which converts ATP to cAMP

24
Q

Where is thromboxane produced?

A

Endothelial Cells - same pathway as for production of prostacyclin
Platelets - TXA2 binds to TPalpha receptor on platelet -> activates platelet -> makes them sticky + produce more TXA2

25
Q

What are the two types of receptor for thromboxane and where are they found?

A 
TPAlpha = Platelets 
TPBeta = Smooth Muscle Cell
26
Q

Describe the mechanism of action of thromboxane on vascular smooth muscle cells.

A

Thromboxane diffuses through apical and basement membranes of endothelial cell then binds to TPBeta receptor on VSMC and activates PLC which finds PIP2
PIP2 —> IP3 + DAG
IP3 induces calcium release from SER
Increase in Ca2+ which activates MLCK –> VASONCONSTRICTION

27
Q

What is the role of the endothelial cell in TXA2 synthesis?

A

Major source for PGH2

28
Q

What is TXA2’s VSMC second messenger?

A

PLC which converts PIP2 to IP3

29
Q

How is endothelin-1 (ET-1) produced?

A

Endothelial cell nucleus produces zymogen Big Endothelin-1. This is converted to endothelin-1 by enzyme Endothelin Converting Enzyme (ECE).

30
Q

What two types of receptors does endothelin-1 have? Where are they situated?

A

ETA - on the VSMC
ETB - on the endothelial cell and VSMC
Endothelin-1 diffuses out of endothelial cell after its production and then can bind same cell or go on VSMC

31
Q

What is the mechanism of action of endothelin-1 on VSMC?

A

ET1 binds to ETA or ETB on VSMC

Receptor releases PLC which converts PIP2 to IP3 which triggers Ca2+ influx –> cell CONTRACTS

32
Q

What is the mechanism of action of endothelin-1 on endothelial cell and then VSMC?

A

ET1 binds to ETB on endothelial cell
This upregulates eNOS so NO is produced.
NO will diffuse into VSMC and induce cell relaxation.

33
Q

What is ET-1’s precursor? What enzyme is used to convert it to ET1?

A

Big Endothelin-1 converted by ECE to ET1

34
Q

What is the role of the endothelial cell for ET1?

A

Precursor source and enzyme source

35
Q

What is ET-1’s VSMC 2nd messenger system?

A

PLC which converts PIP2 to IP3

36
Q

Describe the production of angiotensin II.

A

Renin is released by juxtaglomerular cells
Renin converts angiotensinogen (produced by the liver) to angiotensin I
Angiotensin I is converted to Angiotensin II by ACE (mostly found in the lung endothelium)

37
Q

What effects do angiotensin II have?

A

Increase Vascular Resistance:
Vasoconstriction
Increase sympathetic activity

Increase Water Retention:
Increase sodium reabsorption
Increase vasopressin (aka ADH) secretion
Increase aldosterone production

–> this all contributes to increase BP

38
Q

What other action does ACE have other than converting angiotensin I to angiotensin II?

A

It breaks down bradykinin into bra + dyki + nin

39
Q

Describe angiotensin II’s mechanism of action

A

Diffuses through endothelial cell. Binds to AT1 receptor on VSMC.
PLC converts PIP2 to IP3 which will induce contraction.

40
Q

What is the mechanism of action of bradykinin on endothelial cells and what effect does it have?

A

Bradykinin binds to its receptor on endothelial cells (B1) when ACE is not breaking it down.
PLC: PIP2 —-> IP3 + DAG
Results in UPREGULATIONG OF eNOS —–> increase in NO —–> VASODILATION
This is the opposite effect of ANG-II

41
Q

Describe the mechanism of action of aspirin

A

Apirin permanently disables COX enzymes and subsequent prostaglandin synthesis (platelets can’t recover, endotherlial cells produce new enzymes)
Aspirin is a NSAID

42
Q

Describe the mechanism of action of nitrovasodilators

A

Medication that includes a NO functional group
Donates ‘redy-to-use’ NO
This will difuse into VSMC and have effect
Used to treat angina (too short action to use for HT)

43
Q

Describe the mechanism of action of calcium channel blockers

A

Blocks the flow of channel into cells and so subsequently contraction and so decreases BP.

44
Q

What is the problem with designing calcium channel blockers and what is the solution?

A

A calcium channel blocker needs to be designed such that it doesn’t interfere with the calcium channels in the heart.
Solution: the affinity of the calcium blocker to the channel is dependent on MEMBRANE POTENTIAL
Smooth muscle cells have a MORE POSITIVE membrane potential than cardiomyocytes

CVS (18 decks)

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