Cardiovasular Components

Question 1

Endothelium (ED)

Answer 1

A monolayer of endothelial cells lining the blood interface throughout the CVS including cardiac chambers.

Question 2

Glycocalyx

Answer 2

A carbohydrate-rich protective layer covering the ED, regulates permeability, controls NO production and acts as a mechanosensor of blood shear stress.

Question 3

Endothelium Functions

Answer 3

• Semi-permeable barrier
• Regulates vascular tone
• Enzymes
• Angiogenesis
• Haemostasis
• Immune Defence

Question 4

ED: Semi-permeable barrier

Answer 4

Role in fluid balance, host defence and selective movement of substances e.g., glucose and oxygen.

Question 5

ED: Regulates vascular tone

Answer 5

Secretes vasodilators (e.g., NO) and vasoconstrictors (e.g., endothelin).

Question 6

ED: Enzymes

Answer 6

Contains angiotensin-converting enzyme (ACE) ―plays a key role in regulating blood pressure.

Question 7

ED: Angiogenesis

Answer 7

ED cells are the origin of all new blood vessels.

Question 8

ED: Haemostasis

Answer 8

The luminal surface of ED prevents platelet adherence and coagulation (non-thrombotic, anticoagulant).

Question 9

ED: Immune defence

Answer 9

Healthy ED cells deflect leukocyte adhesion and oppose local inflammation.

Question 10

Vascular smooth muscle cells (VSMCs)

Answer 10

• Located in the tunica media and play a key role in vessel contraction and dilation (regulate blood circulation and pressure).
• With the ED, VSMCs maintain the integrity and elasticity of blood vessels whilst limiting immune cell infiltration.
• Under pathological conditions (e.g., inflammation, oxidative stress, telomere damage) VSMCs undergo phenotypic modulation, altering cell structure and function.
• These changes are central to vascular disease, especially atherosclerosis and hypertension.

Question 11

Role of Nitric Oxide

Answer 11

• NO regulates vascular tone, reduces platelet aggregation and VSMC proliferation, inhibits leukocyte adhesion and inflammatory cytokines, and opposes oxidationof LDLs.
• It is continuously generated from L-arginine by the ED enzyme eNOS.
• NO diffuses easily from the ED into VSMCs and the bloodstream, exerting its main physiological effects in large vessels.
• Vitamin D regulates NO synthesis by mediating eNOS.
• Reduced NO contributes to atheroma formation and CVD.

Question 12

Endothelial Cells: Normal

Answer 12

• Impermeable to large molecules, anti-inflammatory, deflects leukocyte adhesion.
• Enhances vasodilation.
• Resists thrombosis.

Question 13

Endothelial Cells: Activated

Answer 13

• ↑ permeability, inflammatory cytokines and leukocyte adhesion.
• Reduced vasodilator (NO, prostacyclin) molecules.
• Increased risk of thrombosis.

Question 14

VSMCs: Normal

Answer 14

• Normal contractile function, maintains extracellular matrix.
• Contained within the tunica media.

Question 15

VSMCs: Activated

Answer 15

• Increased inflammatory cytokines and extracellular matrix synthesis.
• Migration into the tunica intima and proliferation of VSMCs.

Question 16

Peroxisome proliferator-activated receptor (PPARs)

Answer 16

• PPARs ―nuclear transcription factors that control gene expression involved in adipogenesis, lipid and glucose metabolism, cellular proliferation and apoptosis.
• PPARs decrease inflammation and promote ED health.

Question 17

PPARα

Answer 17

↑HDL-C, ↓TGs and inflammation and is anti-atherosclerotic.

PPAR-α agonists include green tea, resveratrol (up to 50 mg), dietary inclusion of oregano, thyme and rosemary, naringenin (part of citrus bioflavonoid up to 100mg/day) andomega-3 (up to 3 g).

Question 18

PPAR-γ

Answer 18

Reduces blood glucose, fatty acids and insulin. Natural PPAR-γagonists include apigenin, hesperidin, curcumin,** resveratrol, EGCG (polyphenol from green tea).**