Vascular Biology Flashcards

1
Q

As arteries get smaller the velocity increases/decreases.

A

decreases –> cross sectional area –> promotes nutrient exchange

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2
Q

The amount of work that must be done to overcome friction between adjacent layers of fluid sliding over each other

A

shear force

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3
Q

Dilation of blood vessel after a period of ischemia is called:

A

hyperemia

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4
Q

Arteries that carry blood from the aorta to branch arteries

A

conduit arteries

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5
Q

Arterioles vasoconstrict/vasodilate in response to ischemia

A

vasodilate

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6
Q

Do large conduit arteries vasodilate to ischemia?

A

yes: 12-15%

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7
Q

4 molecules that promote vasodilation

A

NO/EDRF, prostacyclin (PGI2), bradykinin, acetylcholine

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8
Q

How does NO lead to vasodilation?

A

L-arginine is involved in production of eNOS (endothelial NO synthase) –> NO diffuses into smooth muscle cell –> activation of cGMP

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9
Q

How does Ach, substance P, bradykinin, B2 agonists lead to vasodilation?

A

G protein calmodulin pathway –> production of eNOS –> NO diffusion to smooth muscle cell –> cGMP

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10
Q

2 effects of ACh on blood vessels

A
  1. stimulates release of NO from endothelium leading to vasodilation
  2. vasoconstriction/contraction in circumstances with low NO (e.g. damaged endothelium) or with high doses of ACh (even low levels of ACh can cause constriction in diseased arteries)
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11
Q

High ACh + low NO causes vasoconstriction/dilation

A

vasoconstriction

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12
Q

Which is more potent? NO or PGI2

A

NO

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13
Q

Angiotensin is a vasoconstrictor/dilator

A

constrictor –> breaks down bradykinin thereby preventing vasodilation by reducing production of NO and and PGI2

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14
Q

A high fat diet impairs endothelial mediated vasodilation/vasoconstriction for up to four hours after eating.

A

vasodilation

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15
Q

What is the difference between an angioblast and an endothelial progenitor cell?

A

angioblast is in utero and epc is what is modified during adulthood to create new vessels –> all under control of VEGF

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16
Q

What factors stabilize growing blood vessels?

A

angiopoetin 1 and ephrin b2

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17
Q

What are 3 important growth factors for vessels?

A

pdgf, tgf beta, fgf

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18
Q

What growth factor can destabilize growing vessels leading to possible tumorigenesis?

A

angiopoetin 2

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19
Q

EPCs from patients with type II diabetes mellitus are characterized by:

A

decreased proliferation capacity and reduction of their adhesiveness and ability to form capillary tubes in vitro

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20
Q

What autosomal dominant condition can result from disruption of TGF beta signalling via abnormalities in one of two genes, endoglin (Eng) and activin-receptor-like kinase-1
(ALK1)?

A

HHT/Osler-Weber-Rendu

21
Q

4 consequences of HHT

A
  1. GI bleeding
  2. infection from septic emboli
  3. arteriovenous malformation in lungs causing shunting of blood and paradoxical emboli
  4. telangiectases
22
Q

3 classifications of anti-clot systems

A
  1. fibrinolytic - t-PA
  2. antithrombin - thrombomodulin, heparin
  3. antiplatelet - NO, prostacyclin, ADPases
23
Q

2 classifications of pro-clot systems

A
  1. anti-fibrinolytic - PAI1

2. angiotensin II stimulation of PAI1 (plasminogen activator inhibitor)

24
Q

_____ cleaves fibrin to produce progressively smaller degradation products

25
Virchow's triad
hypercoagulable state, endothelial injury, circulatory stasis --> clotting/DVT
26
2 procoagulable properties of dysfunctional endothelium leading
1. increase vwf production with increased platelet adhesion/aggregation 2. increased synthesis of PAI1 resulting in impaired fibrinolysis
27
All cell adhesion molecules are constitutively expressed on endothelium except:
ICAM II
28
Migration of neutrophils, monocytes and lymphocytes from the circulating blood to the inflammatory sites is directed by the expression of specific _____ on the endothelium
cell adhesion molecules
29
______ is a transcription factor involved in the expression of genes encoding many proinflammatory functions of vascular wall cells and infiltrating leukocytes.
NFkB
30
_________ acts as a proinflammatory factor by stimulating NFkB leading to expression of _____, which mediates monocyte adhesion and of the chemokine _____, which attracts monocytes
Angiotensin-II, VCAM-1, MCP-1
31
Angiotensin-II stimulates expression of | ______, which provokes the acute-phase response leading to production of the systemic inflammatory marker _________..
interleukin (IL)-6, C-reactive protein | CRP
32
Studies in hypercholesterolemic rabbits have | shown that ____ localizes in endothelium over foam cell–filled fatty streaks in the aorta.
VCAM
33
T/F Endothelial leukocyte adhesion molecules play an important role in early plaque development
T
34
____ stimulates production of endothelial | leukocyte adhesion molecules early in atherosclerotic lesion formation
OxLDL aka oxidative fat
35
Spiral secondary flows and recirculation zones with lower shear stress result in round/elongated endothelial cells
round
36
Do blood vessels have cholinergic innervation?
no --> only muscarinic receptors
37
What stimulates NOS to produce NO from L-arginine?
shear stress, chemical mediateors like ACh
38
Name a competitive inhibitor of L-arginine that indirectly inhibits NO production
ADMA
39
What stimulates PGI2 release from endothelium?
shear stress, physiologic agonists, pathologic insult --> inhibits platelet activation, secretion, aggregation and maintains relaxation
40
Vasoconstrictor or vasodilator? TxA2
constrictor
41
Vasoconstrictor or vasodilator? PGI2
dilator
42
Vasoconstrictor or vasodilator? NO
dilator
43
Vasoconstrictor or vasodilator? endothelin
constrictor
44
Vasoconstrictor or vasodilator? ACh
constrictor
45
Vasoconstrictor or vasodilator? Angiotensin II
constrictor
46
Vasoconstrictor or vasodilator? bradykinin
dilator
47
Vasoconstrictor or vasodilator? substance P
dilator
48
Vasoconstrictor or vasodilator? superoxide anion O2-
constrictor
49
What happens to the number of EPCs in patients with risk factors for ischemic cardiovascular disease?
reduce number of endothelial preogenitors