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Cardiovascular System > Blood vessel order, function and cell specialisation > Flashcards

Blood vessel order, function and cell specialisation Flashcards

1
Q

What are the three layers of blood vessels?

A

Tunica adventitia
• External layer containing blood vessels, 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

What are the function of endothelium?

A
  • Vascular tone management – secretes and metabolises vasoactive substances – this can cause vasoconstriction or vasodilation (balance)
  • Thrombostasis – secretes anti-coagulant substances (prevents clots or molecules sticking to the vessel)
  • Absorption + Secretion – allows diffusion etc.
  • Barrier – prevents entry of bad substances, preventing atherosclerosis formation
  • Growth – mediates cell proliferation
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3
Q

What do mechanoreceptors in endothelial cells do?

A

Detects increased blood flow – secretion of vasodilators

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4
Q

Name 2 types of vasodilators

A

Nitric Oxide – inhibits platelet aggregation

PGI2 (Prostacyclin) – inhibits platelet aggregation and cardioprotective molecule

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5
Q

Name 3 types of vasoconstrictors

A

TXA2 (Thromboxane) – made by endothelial cells and platelets – activates other platelets

ET – 1 (endothelin 1) – can cause constriction and dilation due to different receptors on diff tissues

Angiotensin II

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6
Q

What is an example of a stressor that upregulates NO production?

A

Shear stress force of blood going across the endothelial cells

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7
Q

How does Nitric Oxide work?

A
  • NO production stimulator binds to G-protein coupled receptor
  • Activation of Phospholipase C
  • PLC converts PIP2 to IP3 and DAG
  • IP3 moves to ER and stimulates calcium efflux
  • Leads to upregulation of endothelial nitric oxide synthase (eNOS)
  • eNOS catalyses the following conversion: L-arginine + Oxygen —–> L-citrulline + NO
  • NO exits the endothelial cell and moves to the smooth muscle cell
  • Here it upregulates the activity of Guanylyl Cyclase which converts GTP to cGMP
  • cGMP upregulates Protein Kinase G which leads to relaxation of smooth muscle (calcium efflux reduces tension within the myocyte and stimulates relaxation)
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8
Q

How does ACh cause vasodilation?

A

It triggers the upregulation of endothelial nitric oxide - you get steady vasodilation

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9
Q

If the endothelium is destroyed which drug can be given to cause vessel dilation?

A

SNP – a nitric oxide donor

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10
Q

What is arachidonic acid made from and by what?

A

Phospholipid can be converted to arachidonic acid by Phospholipase A2

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11
Q

What two things can be made from arachidonic acid?

A

• Arachidonic acid can be converted to PGH2 by the COX enzymes (COX = cyclooxygenase)
• PGH2 is a precursor which can be exposed to a variety of enzymes to produce different products
• PGH2 can either becomes:
Prostacyclin (PGI2)
By Prostacyclin Synthase

  Thromboxane A2 (TXA2)
  By Thromboxane Synthase
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12
Q

What is the role of thromboxane?

A
  • It is a powerful vasoconstrictor and it stimulates platelet aggregation
  • It enables the formation of atheromatous plaques
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13
Q

Which receptors does thromboxane bind to?

A
  • Alpha - platelets

* Beta - vascular smooth muscle cells

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14
Q

How does thromboxane lead to vasoconstriction?

A
  • Binds to the beta receptor which is coupled with phospholipase C
  • Converts PIP2 to IP3 which results in the constriction of blood vessels
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15
Q

How does thromboxane lead to platelet aggregation?

A

When thromboxane binds to the alpha receptors on platelets it results in the activation of platelets and the production of more thromboxane which has a domino effect on other platelets and stimulates aggregation

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16
Q

What is the role of prostacyclin?

A
  • Causes vasodilation
  • Inhibits the formation of atheromatous plaques
  • Stops platelet aggregation
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17
Q

Where is COX 1 expressed?

A

in all cells

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18
Q

What happens to COX 2 during inflammation?

A

It will be upregulated

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19
Q

What happens when arachidonic acid follows the leukotriene pathway?

A
  • If arachidonic acid follows the lipoxygenase enzyme cascade you end up with LTD4 and others
  • LTD4 causes bronchoconstriction - associated with asthma
  • Montelukast therapy can reduce bronchoconstriction helping the patient breathe more comfortably
20
Q

Where else can arachidonic acid be produced from?

A

From DAG via DAG lipase

21
Q

What happens if arachidonic acid is exposed to lipoxygenase?

A

Goes down the leukotriene route

22
Q

What happens if arachidonic acid is exposed to COX?

A

It goes down the prostaglandin route

23
Q

How does prostacyclin lead to vasodilation?

A
  • Produced inside endothelial cells
  • Binds to the IP receptor
  • Adenylate cyclase activated which converts ATP to cAMP
  • cAMP upregulates Protein Kinase A
  • Results in relaxation of the vascular smooth muscle causing vasodilation
24
Q

Where else is prostacyclin released and what are its effects?

A

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

25
Q

Where is endothelin – 1 produced?

A

In the nucleus, an endothelin precursor is produced which is then cleaved by Endothelin Converting Enzyme (which is embedded in the membrane) to produce endothelin-1

26
Q

Where does endothelin -1 bind on smooth muscle?

A
  • Alpha and beta receptors on smooth muscle

* They are bound to PLC which converts PIP2 to IP3 which causes contraction

27
Q

What happens if endothelin- 1 binds to beta receptors on an endothelial cell?

A
  • It triggers the activation of eNOS
  • eNOS converts L-arginine and oxygen to L-citrulline and Nitric Oxide
  • Nitric Oxide then moves into the smooth muscle cells and stimulates relaxation
28
Q

Name antagonists which inhibit the production of the endothelin-1 precursor

A
  • Prostacyclin
  • Nitric Oxide
  • ANP (atrial natriuretic peptide)
  • Heparin
  • HGF (hepatocyte growth factor)
  • EGF (epidermal growth factor)
29
Q

Name agonists which stimulate the production of the endothelin-1 precursor

A
  • Adrenaline
  • Vasopressin
  • Angiotensin II
  • Interleukin-1
30
Q

How does angiotensin lead to vasoconstriction?

A
  • Angiotensin II will bind to an angiotensin receptor on vascular smooth muscle cells
  • Leads to activation of PLC and conversion of PIP2 to IP3 resulting in contraction
  • This is because IP3 causes calcium influx which will increase the amount of cross-bridge cycling that takes place
  • Some AT receptors are G-protein coupled but are instead bound to SRC which can upregulate the growth of vascular smooth muscle cells (this may also have some effect on contractility)
31
Q

What is bradykinin and how does ACE affect it?

A
  • It stimulates vasodilation
  • Bradykinin can bind to the bradykinin receptor-1 and activate PLC which converts PIP2 to IP3 which upregulates the production of Nitric Oxide (due to a rise in intracellular calcium)
  • Nitric Oxide then moves to the smooth muscle and causes relaxation
  • Ace breaks down bradykinin so that angiotensin 2 has its desired effect
32
Q

To increase blood vessel diameter, what must be increased and how?

A

• Amount of nitric oxide
• This can be done by:
- Stimulating the production of nitric oxide (endothelium dependent)
- Donating nitric oxide (endothelium independent)

33
Q

Why would you donate NO to a person with microvascular disease to increase the vessel diameter and decrease blood flow?

A

Donation of nitric oxide is endothelium-independent

34
Q

Besides stimulating NO production or donating NO, how can we influence NO?

A
  • Enhancing the effects of the nitric oxide that’s already there
  • Stop the degradation of nitric oxide or stop the degradation of some of the steps to make nitric oxide
35
Q

What is the mechanism for Nitric Oxide Donors?

A
  • Both endogenous and exogenous NO will activate Guanylyl Cyclase which converts GTP to cGMP
  • The cGMP then activates Protein Kinase G which causes relaxation
36
Q

How does Viagra work?

A
  • cGMP is converted to GMP by Phosphodiesterase
  • GMP is metabolically inactive (cGMP normally would activate PKG which causes contraction)
  • Viagra is a phosphodiesterase inhibitor
37
Q

What affect does aspirin have on COX enzymes?

A
  • Aspirin causes irreversible inhibition of the COX enzymes

* (NSAIDs cause reversible inhibition of the COX enzymes)

38
Q

What effect does aspirin have on COX1 and COX2?

A

COX1 – inactivation

COX2 - switches its function

39
Q

Why does reducing arachidonic acid conversion to PGH2 (aspirin) have good and bad effects?

A

There is a reduce in the amounts of thromboxane (bad)

There is a decrease the production of prostacyclin

40
Q

Why does low dose aspirin cause prostacyclin level to level off but thromboxane to continue to decrease?

A
  • Thromboxane is predominantly produced in the platelets

* Platelets do not have a nucleus, so they can’t generate more mRNA to produce new proteins to build the enzyme again

41
Q

Why do we have to be careful when blocking calcium channels?

A

they are found in the heart

42
Q

How does smooth muscle cell and cardiomyocyte RMP differ? Why is this useful when it comes to calcium channel blockers?

A
  • Smooth muscle cells have a higher membrane potential (more positive) than cardiomyocytes
  • The affinity of the channel blocker to the channel is related to the membrane potential of target cells
43
Q

How can ACE inhibitors be used to cause vasodilation?

A
  • Inhibits the breakdown of bradykinin

* By decreasing the breakdown of bradykinin, it stimulates relaxation because bradykinin has a vasodilatory effect

44
Q

Why does a damaged endothelium lead to a platelet plug?

A
  • If the endothelium is damaged, it exposes parts of the sub-endothelial layer (usually collagen) which is sticky causing platelets to adhere to it
  • Platelets stick and release thromboxane which stimulates the aggregation of platelets
45
Q

Which drugs involve Gq protein linked receptor (PLC, PIP2, IP3, DAG)?

A
  • Nitric Oxide production
  • Thromboxane action
  • Endothelin 1 action
  • Angiotensin II action
46
Q

Which drugs involve guanylate cyclase (GTP, cGMP, Protein Kinase G)?

A

Nitric Oxide action

47
Q

Which drugs involve adenylate cyclase (ATP, cAMP, Protein Kinase A)?

A

Prostacyclin action

Cardiovascular System (19 decks)

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