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Cardiovascular system > Vascular Endothelium 1 > Flashcards

Vascular Endothelium 1 Flashcards

1
Q

Relate the anatomy and physiology of the heart

A

The heart is a muscular pump, this is required to generate flow

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2
Q

Relate the anatomy and physiology of the arteries

A

The arteries have thick muscular walls to stabilise pulsatile flow

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3
Q

Relate the anatomy and physiology of the capillaries

A

The capillaries have very thin walls to facilitate gas and solute exchange

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4
Q

Relate the anatomy and physiology of the veins

A

One-way valves to maintain unidirectional flow

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5
Q

What happens when the physiology changes

A

The anatomy can also change- seen in angiogenesis.

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6
Q

Describe how blood can act as an endocrine gland

A

The blood is an important endocrine gland and has evolved to respond to different stimuli.

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7
Q

What is meant by the vascular endothelium

A

Single cell layer of cells that acts as the blood-vessel interface
It has a multitude of important functions.

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8
Q

Describe the roles of the endothelium

A

Vascular tone- Secretes & metabolises vasoactive substances (cause smooth muscle contraction or relaxation)
Thrombostasis- Prevents clots forming or molecules adhering to vessel wall
Absorption and secretion- Allows active/passive transport via diffusion/channels
Barrier- Prevents atheroma development & impedes pathogens
Growth- mediates cell proliferation ( angiogenesis or growth of vessels to enable blood to reach blocked area)

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9
Q

Describe the relationship between anatomy and physiology

A

Bi-directional

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10
Q

What does blood vessel regulation depend on

A

Downstream forces, local mediators, with the aim of being normotensive and adequately perfusing tissues (pulling and pushing forces are in equilibrium).

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11
Q

What happens in hypertension

A

Overactive vasoconstrictive mediators.

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12
Q

Explain how we can assess vascular endothelial function using laser Doppler flowmetry

A

Intact endothelium- add Ach- changes size of micro vessels until plateau is reached.
No endothelium- addition of Ach produces no change in size of micro vessels
Sodium nitroprusside delivery
(exogenous NO-donor)- delivery of Ach changes the size of the micro vessels

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13
Q

What gives blood its colour

A

Haemoglobin- it is a pigment. Oxyhaemoglobin in arteries- bright red
In veins- dark burgundy

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14
Q

How can flow-mediated dilatation be used to assess vascular endothelial function

A

Place cuff around forearm, inflate to around 300mm Hg to occlude the brachial artery- observe how the brachial artery increases in diameter

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15
Q

Why aren’t these methods used to assess endothelial function clinically

A

Observer bias and skill- cross-section of artery in ultrasound, which is 2D, it is hard to locate its position accurately, different positions give different measurements- not strong individually. Too much between-site and observer measurements

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16
Q

Describe the formation of Arachidonic acid

A

Formed from phospholipids in the plasma membrane, catalysed by Phospholipase A2. Can also be formed by different methods

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17
Q

Explain the further reactions of arachidonic acid

A 
Arachidonic acid is converted into PGH2 (precursor for prostaglandins) by COX1 or COX 2. PGH2 can be converted into Prostacyclin (Prostacyclin Synthase).
Thromboxane A2 (Thromboxane synthase)
PGD2, PGE2 and PGF2
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18
Q

What else can arachidonic acid be converted into

A

Leukotrienes (lipoxygenase)

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19
Q

Describe the roles of thromboxane A2

A

Vasoconstrictor
Pro-atherogenic
Pro-platelet
Released in haemostatic crisis

20
Q

Describe the roles of prostacyclin

A

Vasodilator
Anti-atherogenic
Anti-platelet

21
Q

Describe the roles of PGD2, PGE2 and PGF2

A

PAIN, FEVER, INFLAMMATION

22
Q

Describe how nitric oxide can result in relaxation of the smooth muscle

A 
ACh binds to GPCR
PLC migrates along membrane 
PLC converts PIP2 to IP3 (and DAG)
 IP3 triggers Ca2+ influx from ER
Ca2+ upregulates eNOS
eNOS converts L-Arginine and O2 into NO and L- citrulline
NO diffuses into VSMC & activates GC (Guanylyl cyclase)
GC converts GTP to cGMP
cGMP upregulates PKG (Protein Kinase G)
PKG activates potassium channels
Membrane hyperpolarises
Cell Relaxes 
Vessels Dilate

cGMP — GMP by phosphodiesterase

23
Q

Describe the role of shear stress on the relaxation of vascular smooth muscle

A

Shear stress stimulates the activity of eNOS, to dilate the vessel and allow more blood to flow through.

24
Q

Describe the role of prostacyclin on vascular tone

A 
DAG---- Arachidonic acid (DAG lipase)
Arachidonic acid --- PGH2 (COX1, 2)
PGH2 --- PGI2 (prostacyclin synthase)
PGI2 diffuses into VSMC
PGI2 binds to IP receptor
Upregulation of adenylyl cyclase
AC converts ATP to cAMP
cAMP inhibits MLCK
Reduced cross bridge cycling 
Cell relaxes
Vessel dilates
25
Q

Describe the role of Thromboxane A2 on vascular tone

A

TXA2 diffuses through apical and basement membrane
TXA2 binds to TPβ on VSMC
PLC migrates along membrane
PLC converts PIP2 to IP3
IP3 triggers Ca2+ influx from extracellular space and SER
Ca2+ upregulates myosin light chain kinase
VSMC contracts
Vessel Constricts
TXA2 binds to TPα receptor on platelets
Platelet becomes ‘active’ and produces more TXA2
Positive feedback potentiates response
Platelets aggregate

26
Q

Where is thromboxane synthase more widely expressed

A

In platelets

27
Q

Describe the RAAS system

A

Angiotensinogen — Angiotensin 1 (Renin)
Angiotensin 1 —- Angiotensin 2 (ACE, found in lung and kidney endothelium)
Angiotensin 2 - ADH secretion, Aldosterone secretion, Tubular Sodium Reabsorption (Increasing water retention)
Angiotensin 2- Arteriolar vasoconstriction, sympathoexcitaton (Increased Vascular Resistance)

Increased BP

28
Q

Outline how angiotensin 2 can result in vasoconstriction

A 
Ang II diffuses across endothelium
Ang II binds to AT1 receptor
PLC migrates along membrane 
PLC converts PIP2 to IP3 
PLIP3 triggers Ca2+ influx
IP3 triggers Ca2+ influx
Ca2+ upregulates myosin light chain kinase
Cell contracts

ACE metabolises bradykinin
NO-mediated vasodilation is reduced

Vessel constricts

29
Q

Describe the normal actions of bradykinins

A

Bradykinin normally binds to B1 receptors on the endothelium, and stimulates NO production via the PLC pathway

30
Q

Describe the overall effects of endothelin-1

A

Simultaneously causes vasoconstriction and vasodilation , but is predominantly a vasoconstrictor.

31
Q

Describe the vasoconstrictor effects of endothelin-1

A

Endothelial cell nucleus produces Big Endothelin 1
Endothelin converting enzyme converts zymogen to ET-1
ET-1 binds to ETA and ETB receptors on VSMC
Receptors release PLC
PLC converts PIP2 to IP3
IP3 triggers Ca2+ influx
Cell contracts
Vasoconstriction

32
Q

Describe the vasodilator effects of endothelin-1

A 
ET-1 binds to ETB on endothelial cell
Upregulated eNOS
Increased NO production
NO diffuses into VSMC
Cell relaxes
Vessel dilates
These effects are not equal- net effect is vasoconstriction
33
Q

List the antagonists for endothelin-1

A

(PGI2, NO, ANP, heparin, HGF, EGF)

34
Q

List the agonists for endothelin-1

A

Adrenaline, ADH, Ang II, IL-1

35
Q

Which strategy works best to treat hypertension

A

Preventing the influx of Ca2+ into cells- no effect on heart

36
Q

Describe other candidates for anti-hypertensive drugs

A

ACE inhibitors and angiotensin receptor blockers

37
Q

Describe the difference in the expression of COX-1 and COX-2

A

COX-1- constitutively expressed

COX-2- expression is upregulated in times of physiological insult

38
Q

Describe the effect of aspirin on COX-1

A

Aspirin acetylation inactivates enzyme

39
Q

Describe the effect of aspirin on COX-2

A

Aspirin acetylation switches its function (to generating protective lipids)

40
Q

What is the overall effect of aspirin on the COX enzymes

A

Aspirin causes irreversible inhibition of COX enzymes
Other non-specific NSAIDs cause reversible inhibition
COX-2-specific inhibitors cause reversible inhibition of COX-2 isoforms only (don’t know how they differ in efficacy or side effects)

41
Q

Why does aspirin have a greater effect on thromboxane levels than prostacyclin

A

Thromboxane levels decrease more considerably compared to those of prostacyclin.
Prostacyclin is expressed more in the endothelial cells, whereas thromboxane is expressed predominantly in the platelets.
Platelets have no nucleus and thus cannot synthesis more thromboxane (important to wean patients off aspirin before surgery)

42
Q

Describe side effects, adverse reactions and drug-drug interactions

A

Our body often uses the same biochemicals to regulate different processes
Interaction between different systems in the body
Unfortunately, drugs are not always tissue-specific
Receptor expression and distribution varies between tissues
Two people taking the same medicine can have very different experiences
Polypharmacy- people taking too many drugs, interactions with other drugs, genetics and environment

43
Q

Summarise NO

A

Precursor (source) L-arginine (diet)
Enzyme - Endothelial nitric oxide synthase (eNOS
Role of endothelial cell- Source of eNOS
VSMC receptor - none
VSMC 2nd messenger - GTP-CGMP (Guanylyl cyclase (GC)
Relaxation of VSMC
Inhibits platelets

44
Q

Summarise prostacyclin

A

Precursor (source) - Prostaglandin H2 (arachadonic acid; via COX)
Enzyme- Prostacyclin (PGI2) synthase
Role of endothelial cell- Major source of PGH2
VSMC receptor - IP1
VSMC second messenger - ATP to cAMP
(Adenylyl cyclase (AC)
Causes relaxation of VSMC and inhibition of platelets

45
Q

Summarise Thromboxane A2

A

Precursor (source) - Prostaglandin H2 (arachadonic acid; via COX)
Enzyme - Thromboxane synthase
Role of endothelial cell- Major source of PGH2
VSMC receptor - TP1
VSMC second messenger - PIP2 to IP3
(PLC)
Contraction of VSMC and activation of platelets

46
Q

Summarise endothelin- 1

A

Precursor (source) - Big Endothelin-1
Enzyme- Endothelin converting enzyme (ECE)
Role of endothelial cell- Precursor source and enzyme source
VSMC receptor - ETA and ETB
VSMC second messenger - PIP2 to IP3(PLC)
Effects of VSMC- Contraction (main) and relaxation
Effects on platelets - none

47
Q

Summarise angiotensin 2

A

Precursor (source) - Angiotensin I (Angiotensinogen; via Renin)
Enzyme- Angiotensin converting enzyme (ACE)
Role of endothelial cell- ACE expressed on endothelial cell membrane
VSMC receptor- AT1
VSMC second messenger- PIP2 to IP3
(PLC)
Effects on VSMC- Contraction
Effects on platelets- none

Cardiovascular system (19 decks)

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