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CTB > CTB7 - Cell Biology of the Cardiovascular System > Flashcards

CTB7 - Cell Biology of the Cardiovascular System Flashcards

1
Q

What are the three layers of blood vessel wall? Give the location of each.

A

Intima - inner.
Media - middle.
Adventita - outer.

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2
Q

What layer of blood vessel wall is most prominent in the capillaries? Describe.

A

Intima. Contains a single layer of endothelial cells only. Allows for efficient gas exchange.

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3
Q

Describe the difference in thickness (and what contributes to this thickness) between arterial and vein walls.

A

Arteries have thicker walls with greater muscular content. Veins have thinner walls with less muscular content.

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4
Q

What layers are present between the three main layers of the vessel walls?

A

Internal elastic lamina between intima and media.

External elastic lamina between media and adventita.

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5
Q

How do endothelial cells form a barrier?

A

Adhere to one another and overlap. Ensures barrier maintained between blood and vascular wall.

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6
Q

What two properties of endothelial cells are vital for platelets and leukocytes?

A

Smooth and non-adhesive (at most times).

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7
Q

Discuss link between direction/strength of blood flow and the endothelial cells. Why is their orientation preferred in this manner?

A

Stronger blood flow causes elongated flat endothelial cells. These are flattened in the direction of the blood flow - reduces mechanical injury by keeping laminar flow.

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8
Q

Discuss the advantage of endothelial cell overlap is vasculature.

A

Overlap of endothelial cells ensures a strengthened junctions area (junctional proteins). Barrier function is maintained - prevents excessive exchange.

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9
Q

What are the two main types of junctions between endothelial cells?

A

Interendothelial junctions consist of tight junctions and adherens junctions

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10
Q

Which environmental factors cause the release of vasoactive mediators from the endothelium of vasculature?

A

Oxygen tension. Blood flow. Circulating cytokines. Growth factors.

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11
Q

Give examples of vasoactive mediators released by the endothelium. Briefly describe what each does.

A 
Endothelial-1 - vasoconstriction
Norepinephrine - vasoconstriction
Angiotensin I - vasoconstriction
Thromboxane - vasoconstriction
Prostacyclin - vasodilation
Endothelium derived NO - vasodilation
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12
Q

What are the five main functions of the endothelium?

A 
Regulation of vascular tone.
Maintaining barrier function. 
Inflammatory response.
Thrombosis.
Angiogenesis.
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13
Q

What layer largely determines the strength of the blood vessel? What does it contain, that determines the strength?

A

Media. Contains collagen, muscle and elastin ECM.

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14
Q

Discuss differences between the medial layer of the aorta vs the pulmonary artery.

A

Aorta - multiple smooth muscle layers with large amounts of collagen and elastin; ensures high pressure within artery is maintained.
Pulmonary artery - fewer smooth muscle layers with moderate collagen and elastin; ensures few pressure changes occur when large blood volumes are present within the artery

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15
Q

What cells make up the adventita.

A

Collagen. Elastin. ECM. Fibroblasts.

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16
Q

What is the main function of the adventita fibroblasts?

A

Production of structural ECM proteins - involved in vascular compliance

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17
Q

What does the external elastic lamina consist of?

A

Interwoven elastin fibrils.

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18
Q

Discuss the adventita layer within the aortic wall vs the pulmonary artery wall.

A

Aorta - large adventita layer with moderate collagen to elastin amounts; relatively non compliant.
Pulmonary artery - large adventita layer with high collagen to elastin amounts; relatively high compliance.

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19
Q

Discuss what occurs during hot weather to cause skin flushing.

A

Increase in temperature detected by thermosenstiive sensory neurons. Signals sent to thermoregulatory centres in the Brian. Signals sent from the brain to the peripheral blood capillaries to allow vasodilation to occur. Increased blood flow to skin to try to lose more heat - skin flushing occurs.

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20
Q

What is the maximum working distance between the endothelial cells and the smooth muscle?

A

Approx less than 0.5mm

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21
Q

Give three vasoconstrictors and three vasorelaxants.

A

Vasorelaxants - NO, prostacyclin, natriuretic peptides.

Vasoconstrictors - ET-1, angiotensin, thromboxane

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22
Q

Discuss the process by which (endothelium derived) NO induces vasodilation.

A

Endothelial nitric oxide synthase (eNOS) enzymes produce NO from L-arginine (also produces L-citrulline by product). NO diffuses into smooth muscle cells. Activation of soluble guanylate cyclase. GC enzyme converts GTP into cGMP. CGMP causes vasodilation.

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23
Q

What factors causes the activation of eNOS enzymes in vascular endothelial cells?

A

Shear stress. Increased oxygen. Ventilation. Bradykinin and acetylcholine.

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24
Q

What enzymes prevent the vasodilator effect by NO? How do they do this?

A

Phosphodiesterase enzymes inhibit cGMP from causing vasodilation.

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25
Q

In addition to vasodilation, what other effects does NO cause?

A

Inhibits smooth muscle proliferation, inflammation and platelet adhesion.

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26
Q

Discuss the process by which prostacyclin causes vasodilation

A

Prostacyclin is produced by cycloxygenase enzymes from arachnids in acid. It activates IP cell surface receptors. This activates adenylyl cyclase enzymes. They produce cAMP from ATP. CAMP causes vasodilation.

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27
Q

Discuss the process by which prsotacyclin inhibitors vasoconstriction.

A

Prostacyclin activates K+ ion channels. Increased efflux of K+ channels causes membrane hyperpolarisation. Membrane depolarisation temporarily inhibited. No influx of calcium ions into cell. Lack of calcium ions prevents contraction - no vasoconstriction.

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28
Q

What are natriuretic peptides? What stimuli cause the release of natriuretic peptide?

A

Peptide hormones produced by various regions in the Body. Involved in vasodilator effects. Released upon atrial or ventricular distension. Also stimulated by some neurochemical stimuli.

29
Q

Give one key difference between the way in which NO and natriuretic peptides cause vasodilation.

A

Natriuretic peptides activate particulate guanyl cyclase enzymes (membrane bound) as they cannot enter the smooth muscle cell.
NO activates soluble guanyl cyclase enzymes (within the cell) as they can enter the smooth muscle cell.

30
Q

Discuss the process by which natriuretic peptides cause vasodilation.

A

Diffuse through endothelium layer and activate membrane bound particulat guanyl cyclase enzymes on the vascular smooth muscle. GC enzymes convert GTP into cGMP. cGMP causes vasodilator effects.

31
Q

In addition to vasodilation, what other effects do natriuretic peptides have?

A

Lowering of blood pressure - increasing diuretics and natriuesis.
Cardiac relaxation. Anti-fibrotic effects and anti-remodelling effects.

32
Q

Describe the role of ET-1 in causing vasoconstriction.

A

ET-1 produced by endothelial cells and acts on ETA or ETB receptors on the vascular smooth muscle cell. Activation of ETA causes both vasoconstriction and smooth muscle proliferation. Activation of ETB causes vasoconstriction only.

33
Q

Discuss how endothelin-1 may have a vasodilatory effect, in addition to its vasoconstriction effect.

A

If ET1 activates ETA receptors on the endothelium cell, this causes the realise of nitric oxide and prostacyclin. These cause vasodilatory effects via their respective mechanisms.

34
Q

What physical factors and chemical stimuli cause the release of ET-1?

A

Physical factors - shear stress, stretching, hypoxia.

Chemical stimuli - thrombin, epinephrine, angiotensin II, growth factors, cytokines, endotoxins, free radicals.

35
Q

What is the main effect associated with increased plasma levels of ET-1?

A

Vasoconstriction,

36
Q

Discuss the downstream effects caused by angiotensin II via activation of the AT1 receptor.

A

Activation of AT1 causes release of TF, ET-1, ROS and thromboxane.
TF - stimulates coagulation.
ET-1/thromboxane - causes vasoconstriction
ROS - inhibits NO induced vasodilation thus causing vasoconstriction

37
Q

Discuss the downstream effects caused by angiotensin II via activation of the AT2 receptor.

A

Activation of AT2 except or causes release of prostacyclin which has vasodilatory effects.
Activation of AT2 also increases release of bradykinin. Increased activation of bradykinin receptor. Activation of eNOS enzymes. Increased NO production. Increased vasodilatory effects.

38
Q

What is the main effect of angiotensin II induced vasoconstriction?

A

Increased blood pressure

39
Q

Discuss the two main roles of thromboxane and how it exhibits those function.

A

Vasoconstriction. Pro-coagulation.

Increases production of ROS which inhibits NO and so, NO-induced vasodilation.

40
Q

What are four key processes that are controlled by the endothelial barrier function?

A

Tissue-fluid homeostasis. Angiogenesis, vessel tone. Host defence

41
Q

What are the two main pathways involved in endothelial barrier function?

A

Transcellular - through the cell.

Paracellular - through junctions between the cells.

42
Q

What is the function of gap junctions and inter endothelial junctions?

A

Allow the movement of water and ions.

43
Q

What are the two main types of junctions that control the movement of substances through the paracellular pathway, at inter endothelial junctions?

A

Adherens junctions. Tight junctions.

44
Q

Discuss how tight and adherens junctions provide links between cells.

A

Tight and adherens junctions consists of proteins that interact with one another between cells. Within the cell, the junctions are linked to the actin filaments via linker proteins.

45
Q

How are endothelial cells linked to the ECM membrane?

A

Linked via integrins focal adhesions.

46
Q

How do molecules move through the transcellular route?

A

Through use of vesiculo-vacuolar organelles.

47
Q

What are the two forces that control the endothelial barrier function?

A

Contractile and tethering forces.

48
Q

What largely controls the tethering force, that controls endothelial barrier function? What effect does this have on barrier function?

A

Phosphorylation of inter endothelial junction proteins and their associated with actin cytoskeleton within the endothelial cell. Phosphorylated proteins go through conformational changes. Inter endothelial junctions are weakened so weaker cell cell binding. Membrane permeability is increased, barrier function decreased

49
Q

What largely controls the contractile force, that controls endothelial barrier function? What effect does this have on barrier function?

A

Rearrangement of the cytoskeleton I.e. stress fibres formation. Some stimuli cause the formation of stress fibres. These pull on the junctions which reduces the endothelial barrier function.

50
Q

Give factors that stimulate the production of stress fibres within endothelial cells.

A

Inflammatory mediators - thrombin, histamine, tumour necrosis factor alpha.
Conditions - hypoxia

51
Q

What are stress fibres?

A

Contractile units of actin and myosin.

52
Q

Define the difference between angiogenesis and vasculogenesis.

A

Angiogenesis - formation of new blood vessels via branching of existing blood vessels.
Vasculogenesis - formation of new blood vessels de novo from angioblasts.

53
Q

What types of scenarios or conditions stimulate angiogenesis?

A

Hypoxia. Cancers. Wounds.

54
Q

What are the four main steps of angiogenesis?

A

Breakage of cell-cell adhesions. Degradation of basement membrane. Cell migration. Morphogenesis/coalescence of new vessels.

55
Q

Give five mediators that are involved in the regulation of angiogenesis.

A 
Nitric oxide. 
Integrins. 
Junctional proteins. 
ECM components.
Growth factors - VEGF, TGF-b, FGF, PDGF
56
Q

Give a brief overview of the process of angiogenesis.

A

Angiogenesis stimulus activates the endothelial cell. Filopodia starts to form increasing the cell motility. Tip cell starts to move forward away from the existing position, to form a capillary sprout. Cells behind the capillary sprout also begin to migrate and divide, elongating the sprout. Vesicles within the cells begin to join, forming large internal vacuole - forms lumen of new blood vessels.

57
Q

Briefly discuss the role of angiogenesis in tumour cells.

A

Tumour cells become oxygen deficient if they do not have enough blood vessels supplying them. They release angiogenic stimuli to increase the angiogenesis occurring, forming new blood vessels, feeding rather tumour and allowing it to grow.

58
Q

Briefly discuss how the mechanism of angiogenesis in tumour cells can be targeted as an anti cancer process.

A

Tumour cells grow by releasing lots of angiogenesis stimuli eg various growth factors. Targeting the release of these or causing them to be broken down, preventing tumour cell angiogenesis from occurring, which can tumour death.

59
Q

Discuss the balance of pro and anti coagulants in a normal endothelium.

A

Greater amount of anti coagulants than pro-coagulants. Ensures blood fluidity.

60
Q

Discuss the balance of anti coagulants and pro coagulants in an activated endothelium. When do endothelium become activated?

A

Increased pro coagulants relative to anti coagulants. Occurs during wound healing.

61
Q

Define haemostasis. When is it important?

A

Stopping of blood flow. Vital for damaged blood vessels e.g. wounds.

62
Q

Discuss benefits and disadvantages of fibrinolytic during would healing.

A

Benefits - ensures that risk associated with excess clots is reduced.
Disadvantages - can prevent clot formation at the site of injury

63
Q

Name six endothelium derived anti coagulants

A 
Prostacyclin
NO
Heparan sulphate proteoglycan
Thrombomodulin
TF pathway inhibitor
Tissue type plasminogen activator
64
Q

Name three endothelium deceived pro coagulants.

A

Von willebrand factor.
Tissue factor.
Plasminogen activator inhibitor 1

65
Q

What types of situations would an inflammatory response be required for?

A

Pathogen infections. Cell damage. Irritants. Wounds

66
Q

What are the three processes involved in the inflammatory response?

A

Increased leukocyte extravasation.
Vasoconstriction.
Thrombosis.

67
Q

Give four examples of pro inflammatory cytokines.

A

Colony stimulating factor 1
Monocytes chemostatic protein 1
Interleukins
Chemokine RATNES

68
Q

Give brief overview of the process of leukocyte extravasation.

A

Leukocytes circulating in the blood stream. When they detect an infection or wound, they become sticky and adhere to the capillary well. This is because the leukocytes express sialyl Lewis X and the endothelial cells express selectins. At some point, conformational changes occurs with mean that leukocytes express LFA1 and endothelial cells expresssed ICAM1. These cause tighter binding. The leukocytes then undergo diapedesis and exit the capillary. Located to site of infection/damage via chemical signals.

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