Vascular endothelium Flashcards
three layers for blood vessels except capillaries + venules
tunica advenitia
tunica media
tunica intima
tunica intima
endothelium
tunica media
smooth muscle cells
tunica adventitia
nerves, vaso vasorum (small blood vessels)
How are capillaries + venules different in structure
only formed by endothelium (one cell thick)
other function of microvascular endothelium
promotes tissue homeostasis
how does miscorvascular endothelium promote tissue homeostasis
release angiocrine factors
What can dysfunctional endothelium contribute to
ischemia
chronic inflammatory disease
cancer
diabetes
three types of vessels
non-fenestrated
fenestrated
discontinuous
non-fenestrated
blood brain barrier/ muscle/ lung/ skin
fenestrated
GI tract/ kidney glomerulus
discontinuous
liver/ sinus
Features of the endothelium
Very large SA
Monolayer of endothelial cells (contact inhibition)
Endothelial cells - long life _ low proliferation rate
What do endothelial cells do?
Control multiple functions of blood vessels: vascular tone permeability inflammation thrombosis angiogenesis
Provide angiocrine signals essentials for tissue homeostasis
How are endocrine cells heterogeneous
their function and phenotype depend on their location
what happens during the resting endothelium
anti- factors are switched on (eg. anti-inflammatory/ anti-thrombotic etc)
what happens during the active endothelium
pro- factors are switched on (eg. pro- inflammatory/ pro-thrombotic etc)
What contributes to the development of artherosclerosis
Chronic activation of pro-factors
What 4 factors lead to atherosclerotic plaque
Leukocyte recruitment
permeability
shear stress
angiogenesis
Formation of complicated lesion in artherosclerosis?
Macrophage accumulate and form a necrotic core + angiogenesis
How does leukocyte recruitment contribute to atherosclerosis
Normally takes place during inflammation - adhere to endothelium of post-capillary venules + transmigrate into tissues
In atherosclerosis = leukocytes adhere to activated endothelium of large arteries + get stuck in sub-endothelial space as they cannot transmigrate = contribute to plaque formation
How does increased permeability contribute to atherosclerosis
endothelium becomes leaky when inflamed = lipoproteins slip through and become oxidised = forms foam fat cells
(fatty streak formation)
How does shear stress/ blood flow contribute to atherosclerosis
plaques occur preferentially at bifurcations/ curvatures in vascular network (blood flow is not laminar there = non uniform/ low wall shear stress so more stagnant and less anti-thrombotic)
Blood flow and NO link?
Disturbed flow causes loss of No production (essential for health of CV system - vasodilation/ platelet activation etc)
