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CVS > Vascular Endothelium I > Flashcards

Vascular Endothelium I Flashcards

1
Q

VE?

A

single layer of cells that act as a blood vessel interface

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2
Q

What are the functions of the VE?

A

vascular tone (secrete and metabolise vasoactive substances)
permeability
thrombostasis (prevent clots, adhere to wall)
absorption/secretion ( allow passive/active transport)
barrier (prevent atheroma, impede pathogen)
growth (mediate cell proliferation)
angiogenesis
inflammation

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3
Q

What are the effects of a vasodilator?

A 
smooth muscle 
- relaxation
- inhibit growth
myocytes
- increase blood flow
- increase contractility 
platelets 
- inhibit aggregation
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4
Q

Describe the synthesis of NO

A

endothelium dependent process

  1. GPCR stimulated by ACh activated PLC
  2. converts PIP2 –> DAG + IP3
  3. IP3 stimulate Ca release which activates eNOS enzyme (also by increased shear stress)
  4. eNOS mediates reaction of L-arginine + O2 –> L-citrulline + NO
  5. NO moves into smooth muscle and activates internal guanylyl cyclase to convert GTP –> cGMP
  6. cGMP activates PKG to stimulate relaxation
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5
Q

How does shear stress affect vessel?

A

increase flow rate and velocity
increase shear stress and increase friction
stimulate NO synthesis
vasodilation

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6
Q

What is the effect of NO on larger vessels?

A

smaller

increase diffusion distance

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7
Q

What is the difference between endothelium dependent and flow mediated vasodilation?

A

ED - ACh stimulates NO production

FM - if vessels occluded, NO release necessary

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8
Q

What are the effects of prostacyclin (PGI2)?

A

vasodilator

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9
Q

What are the effects of thromboxane (TXA2)

A

vasoconstrictor

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10
Q

Describe the synthesis of PGI2 and TXA2?

A 
phospholipids --> arachidonic acid (PLA)
--> PGH2 (COX1 and COX2)
--> TXA2 (thromboxane synthase)
--> PGI2 (prostacyclin synthase)
COX1 constitutively expressed but COX2 expression induced by inflammatory mediators only

PGH2 –> PGD2, PGE2, PGF2 (pain, fever, inflammation)

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11
Q

What does aspirin target?

A

COX1 and COX2

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12
Q

Describe the activity of PGI2?

A
  1. PGI2 binds to IP1 receptor on smooth muscle
  2. activates internal adenylyl cyclase
  3. ATP –> cAMP
  4. cAMP inhibits MLCK
  5. reduced cross bridge cycling –> vasodilation
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13
Q

Describe the activity of TXA2?

A

BASAL

  1. TXA2 diffused through membrane and binds to TPB receptor
  2. PLC migrates along membrane and converts PIP2 –> IP3
  3. IP3 triggers Ca release and up-regulates MLCK
  4. vasoconstriction

APICAL

  1. TXA2 binds to TPalpha receptor on platelets
  2. platelets more active
  3. produce more TXA2
  4. positive feedback potentiates response
  5. platelets aggregate
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14
Q

Where is the core site of TXA2 synthase enzyme?

A

platelets more than endothelial cells

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15
Q

What is endothelin I (ET-1)?

A

vasoconstrictor
(can vasodilate depending on the receptor)
minor effect = stimulate growth

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16
Q

What is angiotensin II?

A

vasoconstrictor

17
Q

What are antagonists of ET-1?

Agonists?

A

PGI2, NO, ANP, heparin, HGF, EGF

adrenaline, ADH, AngII, IL-1

18
Q

What is the mechanism of action of ET-1?

A
  1. Agonists/antagonists pass into endothelial cell nucleus
  2. ECE enzyme converts zymogen (Big ET-1) to ET-1 that is produced by the nucleus
  3. ET-1 diffuses across basal layer

VASOCONSTRICTION

  • ET1 binds to ETA and ETB on VSMC (paracrine)
  • converts PIP2 –> IP3
  • cause Ca influx
  • stimulate MLCK

VASODILATION

  • ET1 has autocrine effect
  • bind to ETB on endothelial cell
  • stimulate eNOS production to make NO for vasodilation

MAJOR EFFECT IS VASOCONSTRICTION

19
Q

How does angiotensin II work?

A

via renin-angiotensin-aldosterone axis

  1. renin cleaves angiotensinogen to Ang I
  2. ACE converts it to Ang II
  3. Ang II increases vascular resistance (TPR)
  4. bind to AT1 receptor to increase water retention
  5. 3 and 4 increase BP
20
Q

What is renin?

A

an enzyme

21
Q

Where is ACE located ?

A

on endothelial lining

22
Q

When is RAA good?

A

if bleeding to death

maintain circulating volume at adequate BP

23
Q

What stimulates increased vascular resistance?

A

arteriolar vasoconstriction
sympathoexcitation
both increase CO –> vasoconstriction

24
Q

What stimulates increased water resistance?

A

tubular Na reabsorption

ADH and aldosterone secretion

25
Q

What does ACE enzyme also mediate?

A 
metabolism of bradykinin (vasodilator)
oxidative stress
inflammation 
remodelling
endothelial dysfunction
26
Q

Describe drug supplements for NO?

A

endo dependent

  • GPCR binding compound infusion (ACh)
  • phosphodiesterase inhibitors/inhibit cholinesterase to lengthen effects of NO and prevent NO metabolism
  • block flow of Ca into cells to stop Ca dependent cross bridge cycling

endo independent
- NO donating drugs (glyceryl trinitrate GTN) to provide exogenous NO, e.g. NITROVASODILATORS (too short acting), GTN spray for angina but can cause fainting by decreasing BP too fast

best option: affect vasculature and not heart

27
Q

How does viagra work?

A

inhibits PDES that turns cGMP to CMP thus avoiding end of vasoconstriction

28
Q

Describe the action of aspirin?

A
  • inactivates COX1 and switched COX2 function to generate protective lipids
  • levels of TXA2 reduced (made in platelets with 7-9 day lifespan, no nucleus to make more COX enzyme)
  • PGI2 still high as made in endo cells and can regenerate COX enzyme
29
Q

How do non specific NSAIDs work?

A

reversible inhibition

30
Q

How is COX1/2 expressed?

A

COX 1 - constitutive expression

COX 2 - expressed after physiological insult

31
Q

How is cytosolic Ca regulated?

A

block VGCC can block vasoconstriction (amyloDIPENE)

- VGCC blockers may be specific (will not stop heart) by only binding to cells with specific membrane potentials

32
Q

What are examples of antihypertensive medication?

A

angiotensin receptor blockers (ARBs) - SARTSAN

ACE inhibitors that disable endothelial expression of ACE - PRIL

CVS (16 decks)

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