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Reg Phys and Pharm > Regulation of Blood Flow and Blood Pressure > Flashcards

Regulation of Blood Flow and Blood Pressure Flashcards

- Describe the structure of a blood vessel and identify the cellular components - Understand the mechanisms by which the body can regulate blood flow and pressure - Discuss the key signalling pathways involved in vascular function and explain how these go wrong in disease - Explain current pharmacological strategies to improve vascular reactivity and blood flow

1
Q

The function of blood vessels

A

Carry blood around the body towards target organs and tissues

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2
Q

Systemic arteries, arterioles and capillaries

A

carry oxygenated blood and nutrients from left ventricle towards systemic organs

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3
Q

Systemic veins, venules, and capillaries

A

deoxygenated blood and waste from periphery towards the right atria

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4
Q

Pulmonary blood vessels

A
  • reoxygenation of blood at the lungs
  • returned to heart for circulation
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5
Q

function of intima (endothelial cells and subendothelial space)

A
  • single-cell layer
  • first barrier to pathogens in the blood
  • communicates with vascular smooth muscle to regulate diameter
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6
Q

function of the media (vascular smooth muscles)

A

relaxation/constriction dictates vessel diameter

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7
Q

Adventitia/externa

A
  • outer layer of fibrous connective tissue surrounding an organ
  • collagen rich
  • external elastic lamina
  • vaso vasorum
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8
Q

Vessel diameter

A

regulates blood flow and pressure

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9
Q

Layers of arteries and arterioles

A

intimal, medial, and externa elastic

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10
Q

Function of valves

A

Prevent backflow of blood

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11
Q

Difference between veins and arteries and arterioles

A

veins and venules lack elastic layers

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12
Q

Key hormones in regulation of vasular tone

A
  • nitric oxide
  • endothelial derived hyperpolarising factor
  • endothelin-1
  • angiotensin II
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13
Q

Production of nitric oxide

A
  • stimulation of GPCR by ligand creates multiprotein cascade
  • production of IP3 which acts on the ER to singal release of intracellular calcium
  • calmodulin activation -> phosphorylation and activation of nitric oxide synthase (ENOS)
  • ENOS catalyses the conversion of L-Argenine to L-Citruline
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14
Q

How does nitric oxide cause smooth muscle contraction

A
  • activation of guanylyl cyclase
  • converts GTP to GMP
  • activation of PKG
  • relaxation of muscle fibres
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15
Q

Endothelial derived hyperpolarising factor (EDHF)

A
  • hyperpolarises smooth muscle via stimualtion of potassium efflux
  • muscle relaxation
  • important when NO production is compromised
  • acts predominantly at the arteriole level
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16
Q

Endothelin-1

A
  • acts on smooth muscle to induce vasoconstriction via smooth muscle intracellular calcium release
  • inhibits eNOS
  • reduces NO bioavailability
  • promotes vascular inflammation
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17
Q

Angiotensin II

A
  • multiple tissue targets
  • smooth muscle constriction via GPCR signalling and intracellular calcium release
  • excessive levels promote high blood pressure and vascular inflammation
18
Q

Metabolic syndrome diagnostic criteria

A
  • insulin resistance
    and any two of:
  • obesity
  • dyslipidaemia
  • raised blood pressure
  • raised blood glucose
19
Q

Atherosclerosis

A

progressive thickening and hardening of medium to large sized arteries as a result of fat deposition on the inner lining

20
Q

5 key stages of atherosclerosis

A
  1. endothelial dysfunction
  2. immune cell infiltration
  3. fatty streak
  4. young plaque
  5. unstable plaque
21
Q

Endothelial dysfunction

A
  • can be measured as indicator of atherosclerosis risk
  • begins in response to cardiovascular risk factors and chronic inflammation
  • loss of endothelium-derived vasomotor control (decreased NO production, increased ET-1)

Characterised by
- increased expression of adhesion molecules
- increased chemokine and cytokine secretion
- increased cell permeability
- increased LDL oxidation

22
Q

Immune cell infiltration

A
  • infiltration of the sub-endothelial space by immune cells and ox-LDL

Characterised by
- increased adhesion molecules present on endothelial cells
- initial recruitment of monocytes/macrophages
- followed by other immune cells (T and B cells, neutrophils and dendritic cells)

23
Q

Fatty streak

A
  • further accumulation of ox-LDL and phagocytosis of ox-LDL by macrophages
  • visible as yellow fatty streak on vessel lumen
  • lipid droplets form in vascular smooth muscle cytoplasm
  • smooth muscle and fibroblast proliferation and migration
  • dysregulated signalling of ET-1, NO, and Ang-II
24
Q

Young plaque

A
  • accumulation of ‘foam cells’ and thinning of fibrous cap
  • foam cells cluster, creating hypoxic central core (becomes neurotic)
  • fibrous cap of developing plaque thins as lesion grows
  • plaque is stable but narrowing vessel lumen
25
Q

Vulnerable/unstable plaque

A
  • plaque becomes unstable
  • necrotic core
  • calcification
  • likely to rupture, releasing thrombus and occluding vessel
26
Q

How does adipocyte dysfunction promote atherosclerosis

A
  • hyperinflammatory adipocytes release pro-inflammatory cytokines and adipokines
  • contribute alongside: insulin and leptin resistance, increased FFA, and hypercholesterolaemia
27
Q

Dysregulation of AngII in MetS

A
  • increased levels and signalling
  • promotes inflammation and smooth muscle proliferation, resulting in atherogenic environment
28
Q

Dysregulation of ET-1 in MetS

A
  • potent inflammatory peptide - promotes oxidative stress and immune cell recruitment in vessel wall
  • increased production and processing also supresses NO signalling, promoting vasoconstriction
29
Q

Dysregulation of NO in MetS

A

bioavailability of NO reduced via inhibition of eNOS and peroxinitrate production

30
Q

Dysregulation of EDHF in MetS

A

decreased production and transport of EDHFs, impairing vascular responses

31
Q

MetS and CVD

A
  • pathophysiology of CVD and MetS is multifaceted
  • wide array of therapies to treat insulin resistance, inflammation, oxidative stress, cholesterol, hyperglycaemia, hypertension
32
Q

Common therapies for MetS and Atherosclerosis

A
  • Thiazolidinediones (TZDs/Glitazones)
  • HMG-CoA Reductase Inhibitors (Statins)
  • AMPK activators (Biguanides)
  • Antioxidants
33
Q

Thiazolidinediones (TZDs/Glitazones)

A

PPARy agonists
- insulin sensitisers
- increases HDL cholesterol
- anti-inflammatory effect in vessel wall

34
Q

HMG-CoA Reductase Inhibitors (Statins)

A

cholesterol biosynthesis inhibitors
- increases HDL cholesterol levels
- decreases LDL cholesterol levels and oxidation

35
Q

AMPK activators (Biguanides)

A

complex I inhibition
- regulates glucose metabolism
- increases FA oxidation
- reduces inflammation

36
Q

Antioxidants

A
  • reduce ROS
  • reduce LDL oxidation
37
Q

Current therapies for vascular dysfunction

A
  • NO donors
  • ACE inhibitors
  • Endothelin receptor antagonists
  • Endothelin converting enzyme (ECE) inhibitors (currently untested in humans)
  • Surgery
38
Q

NO donors

A

Improves vasoresponsiveness

39
Q

ACE inhibitors

A
  • reduces AngII production
  • alleviates vasoconstriction / favours vasodilation
  • reduces blood pressure
40
Q

Endothelin receptor antagonists

A

limited effectiveness

Reg Phys and Pharm (16 decks)

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