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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
Describe the role of Thromboxane A2 on vascular tone
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
Where is thromboxane synthase more widely expressed
In platelets
27
Describe the RAAS system
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
Outline how angiotensin 2 can result in vasoconstriction
``` 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
Describe the normal actions of bradykinins
Bradykinin normally binds to B1 receptors on the endothelium, and stimulates NO production via the PLC pathway
30
Describe the overall effects of endothelin-1
Simultaneously causes vasoconstriction and vasodilation , but is predominantly a vasoconstrictor.
31
Describe the vasoconstrictor effects of endothelin-1
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
Describe the vasodilator effects of endothelin-1
``` 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
List the antagonists for endothelin-1
(PGI2, NO, ANP, heparin, HGF, EGF)
34
List the agonists for endothelin-1
Adrenaline, ADH, Ang II, IL-1
35
Which strategy works best to treat hypertension
Preventing the influx of Ca2+ into cells- no effect on heart
36
Describe other candidates for anti-hypertensive drugs
ACE inhibitors and angiotensin receptor blockers
37
Describe the difference in the expression of COX-1 and COX-2
COX-1- constitutively expressed | COX-2- expression is upregulated in times of physiological insult
38
Describe the effect of aspirin on COX-1
Aspirin acetylation inactivates enzyme
39
Describe the effect of aspirin on COX-2
Aspirin acetylation switches its function (to generating protective lipids)
40
What is the overall effect of aspirin on the COX enzymes
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
Why does aspirin have a greater effect on thromboxane levels than prostacyclin
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
Describe side effects, adverse reactions and drug-drug interactions
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
Summarise NO
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
Summarise prostacyclin
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
Summarise Thromboxane A2
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
Summarise endothelin- 1
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
Summarise angiotensin 2
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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