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CVS > 6. Blood Vessel Order, Function and Specialisation of Cells > Flashcards

6. Blood Vessel Order, Function and Specialisation of Cells Flashcards

1
Q

What are the 3 layers of blood vessels and their function?

A
  • Tunica adventitia - external layer containing blood vessles, fibrous tissue, elastin and collagen, helps keep the shape
  • Tunica media - predominantly smooth muscle cells - contractions and dilation
  • Tunica intima - predominantly vascular endothelium with the elastic basal lamina - exchange surface
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2
Q

What is the basic anatomy and physiology of the heart, arteries, capillaries and veins?

A

(• structure and function)
• Heart: muscular pump - generate flow
• Arteries: thick muscular walls - stabilise pulsatile flow
• Capillaries: very thin walls - facilitate gas a solute exchange
• Veins: valves - maintain unidirectional flow

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3
Q

What are the 5 functions of the vascular endothelium?

A
  • Vascular tone management - secreting and metabolising vasoactive substances
  • Thrombostasis - secretes anti-coagulant substances
  • Absorption + secretion - transport via diffusion/channels
  • Barrier - prevents entry of bad substances preventing atherosclerosis or further infection
  • Growth - mediates cell proliferation
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4
Q

Name 2 important vasodilators (and their functions)

A
  • Nitric Oxide (NO) - inhibits aggregation of platelets

* Prostacyclin (PGI2) - cardioprotective molcule, inhibits aggregation of platelets

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5
Q

Name 3 important vasoconstrictors (and their functions)

A
  • Thromboxane (TXA2) - produced in endothelial cells and platelets, activates other platelets which stimulates aggregation
  • Endothelin 1 (ET-1) - can cause vasodilation as well as vasoconstriction as it has different receptors on different tissues
  • Angiotensin II (ANG II)
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6
Q

Can vasodilation occur when there’s no endothelium?

A
  • No
  • Despite acetylcholine delivery, the endothelium is needed to produce NO for smooth muscle stimulation
  • However, an exogenous NO-donor (SNP) can bypass this and cause vasodilation
  • Therefore, the endothelial cells don’t need to be relied upon for nitric oxide production
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7
Q

How is arachidonic acid produced?

A
  • Phospholipid (from phospholpid bilayer) => arachidonic acid [phospholipase A2]
  • DAG => arachidonic acid [DAG lipase]
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8
Q

What can arachidonic acid be converted into and why is this done?

A
  • Arachidonic acid => Prostaglandin H2 (PGH2) [cyclooxygenase (COX)]
  • COX 1 is expressed in all cells
  • COX 2 is upregulated if there is an inflammatory problem
  • PGH2 is a precursor to a variety of products
  • Arachidonic acid => Leukotrienes i.e. LTA4, LTB4, LTC4 & LTD4 [Lipooxygenase Enzyme cascade]
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9
Q

What can Prostaglandin H2 converted into and what are their functions?

A
  • Prostacyclin (PGI2) [Prostacyclin Synthase] - causes vasodilation, inhibits atheromatous plaque formation and stops the aggregation of platelets (cardioprotective)
  • Thromboxane A2 (TXA2) [Thromboxane Synthase] - powerful vasoconstrictor and stimulates platelet aggregation (typically bad for CVS)
  • Other products involved in pain, fever, inflammation and the health of the epithelia in the GI tract
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10
Q

What is the function of LTD4 and what is Montelukast therapy?

A
  • Bronchoconstriction
  • Associated with asthma
  • Montelukast therapy can reduce bronchoconstriction
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11
Q

Describe the process from something that stimulates NO production to vasodilation

A
  • Stimulating substance binds to G-protein coupled receptor
  • Phospholipase C activated and moves along the membrane
  • PLC => IP3 and DAG
  • IP3 moves to the endoplasmic reticulum and stimulates calcium efflux
  • Rise in calcium upregulates endothelial nitric oxide synthase (eNOS) which converts L-arginine + oxygen => L-citrulline + NO
  • NO exits endothelial cell and moves to the vascular smooth muscle cell (VSMC)
  • It upregulates the activity of Guanylyl Cyclase which converts GTP => cGMP
  • cGMP upregulates Protein Kinase G - activates potassium channels
  • Potassium flows in - hyperpolarises the membrane - cell relaxes
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12
Q

What does shear stress do to the VSMCs?

A
  • Stimulator of NO production

* Causes vasodilation to reduce damage due to increased pressure

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13
Q

How does Prostacyclin (PGI2) work?

A
  • Produced by PGH2
  • Diffuses into VSMC
  • Binds to IP receptor which is coupled to adenylate cyclase (AC)
  • AC converts ATP to cAMP
  • cAMP upregulates Protein Kinase A, which inhibits Myosin Light Chain Kinase
  • Reduces cross-bridge cycling - relaxation
  • Vasodilation

• Also secreted into blood - anti-platelet aggregation properties

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14
Q

How does Thromboxane (TXA2) work?

A
  • Diffuses out through both the apical and basement membrane
  • Binds to alpha receptor (apical, in platelets) - activation of platelets and production of more thromboxane (positive feedback), domino effect on other platelets, stimulating aggregation until stimulus stops
  • Binds to beta receptor (basal, in VSMCs) - coupled with Phospholipase C
  • PLC converts PIP2 to IP3 (in VSMCs, unlike the action of NO which produces IP3 in the endothelial cell)
  • IP3 triggers calcium influx from extracellular space and SER
  • calcium upregulates myosin light chain kinase
  • VSMC contracts
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15
Q

How is Angiotensin II produced?

A

• Renin secreted from kidneys in response to low blood pressure (low renal perfusion)
• Renin cleaves Angiotensinogen to Angiotensin I
• ACE is expressed on endothelial cells in renal/pulmonary circulation:
it converts Angiotensin I to Angiotensin II

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16
Q

What does Angiotensin II do?

A

Increasing water retention:
• Stimulates ADH secretion
• Increases aldosterone production
• Increases sodium reabsorption

Increasing vascular resistance:
• Increased sympathetic activity (sympathoexcitation)
• Arteriolar vasoconstriction

These both lead to an increase in blood pressure

17
Q

How does Angiotensin II work in endothelial cells and VSMCs?

A
  • Angiotensin II diffuses across endothelium
  • Binds to an angiotensin receptor (AT1) on VSMCs
  • This leads to the activation of Phospholipase C
  • PLC converts PIP2 to IP3
  • IP3 triggers calcium influx from extracellular space and SER
  • calcium upregulates myosin light chain kinase
  • VSMC contracts
  • BP increases
18
Q

What kind of receptors are AT1?

A
  • Some are G-protein coupled receptors
  • Bound to SRC (proto-oncogene) which can upregulate the growth of VSMCs
  • Also a mechanism to increase BP
19
Q

How does bradykinin work and what does ACE do to it?

A

• ACE breaks down bradykinin

  • Bradykinin binds to bradykinin receptor-1
  • This activates PLC
  • This converts PIP2 to IP3 which upregulates the production of NO in endothelial cells (due to a rise in intracellular calcium)
  • NO moves to the VSMC causing relaxation
  • Bradykinin has an opposite effect to Angiotensin II
20
Q

How is Endothelin-1 produced and how does it (mainly) work?

A
  • Endothelin precursor (Big Endothelin 1) is produced in the nucleus of the endothelial cell
  • Cleaved by Endothelin Converting Enzyme into Endothelin-1
  • Endothelin-1 leaves the cell and binds to alpha or beta receptors, both on the VSMCs
  • They are both bound to PLC
  • PLC converts PIP2 to IP3
  • IP3 triggers calcium influx
  • calcium upregulates myosin light chain kinase
  • VSMC contracts
  • This is the main function due to the greater receptor expression
21
Q

What happens in endothelin-1 binds to a beta receptor on the endothelial cell?

A
  • Activation of eNOS
  • Leads to the production of NO
  • NO moves to the VSMC, leading to relaxation
22
Q

What are the agonists which stimulate the production of Endothelin-1 (precursor)?

A
  • Adrenaline
  • Vasopressin
  • Angiotensin II
  • Interleukin-1
23
Q

What are the antagonists which inhibit the production of Endothelin-1 (precursor)?

A
  • Prostacyclin
  • Nitric Oxide
  • ANP (atrial natriuretic peptide)
  • Heparin
  • HGF (hepatocyte growth factor)
  • EGH (epidermal growth factor)
24
Q

What is the best way to induce the relaxation of VSMCs?

A
  • Block the flow of calcium into cells
  • Impedes cross-bridge cycling which is calcium dependent
  • Endothelium-dependent
25
Q

How else can the relaxation of VSMCs be induced and why aren’t they preferable?

A
  • Inhibition of cholinesterase enzymes - reduces the breakdown of ACh, however ACh has many other effects
  • Inhibition of phosphodiesterase enzymes - reduces the breakdown of NO 2nd messenger system, however this has undesirable side-effects
  • Medication including an NO functional group, however it is too short-acting
26
Q

Outline the use of NO being used to induce vessel dilation

A
  • Increase the amount of Nitric Oxide: stimulating production or donating NO e.g. with SNP
  • Stimulation is endothelium-dependent - reliant on cascade to generate NO
  • Donation is endothelium-independent - favourable when there is endothelial damage
27
Q

What is the mechanism for NO donors?

A
  • Both endogenous and exogenous NO activate Guanylyl Cyclase
  • This converts GTP to cGMP
  • cGMP activates Protein Kinase G - relaxation
28
Q

What is the mechanism of Viagra?

A
  • Phosphodiesterase (PDES) converts cGMP to GMP
  • GMP is metabolically inactive
  • So, Viagra is a phosphodiesterase inhibitor
29
Q

What effect do NSAIDs have on COX enzymes?

A

Reversible inhibition

30
Q

What does Aspirin decrease the levels of in the body and how?

A
  • Aspirin causes irreversible inhibition of COX enzymes
  • Inactivates COX1 & switches the function of COX2 to generating protective lipids
  • Reduced conversion of Arachidonic acid => PGH2
  • Less thromboxane and prostacyclin
31
Q

Why is a Low Dose of Aspirin beneficial?

A
  • Prostacyclin has anti-platelet aggregation properties, which we don’t want to lose, so a low dose of Aspirin is used
  • Prostacyclin levels decrease slightly, then that level is maintained
  • Thromboxane activates platelets, which we want to decrease during inflammation
  • Thromboxane is also predominantly produced in platelets, so levels continue to fall, even after a small dose
  • Platelets don’t have a nucleus - no mRNA to produce new enzymes
32
Q

Why don’t calcium channel blockers affect cardiomyocytes?

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
33
Q

How do ACE inhibitors induce relaxation in the VSMCs?

A
  • Inhibit the conversion of Angiotensin I to Angiotensin II => less Angiotensin II
  • Also inhibit the breakdown of bradykinin => more bradykinin
  • Bradykinin has a vasodilatory effect
34
Q

How does a damaged endothelium lead to the formation of a platelet plug?

A
  • Exposed sub-endothelial layer (collagen)
  • Causes platelets to adhere
  • Platelets stick and release thromboxane
  • Stimulates the aggregation of platelets
  • Platelet plug forms

CVS (21 decks)

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