Flashcards in Vascular Biology Deck (24)
Where does the blood pressure vary the most?
In large arteries.
Do endothelial cells respond to changes in shear stress and pressure?
4 vasodilation factors?
What's interesting about the effect of ACh on vascular tone?
If the endothelium is present, ACh causes dilation.
If the endothelium is disrupted, ACh causes constriction.
How do ACh, bradykinin, and beta-2 agonists cause vasodilation?
By stimulating eNOS in endothelial cells to make NO.
NO then acts on smooth muscle cells.
Why does ACh cause smooth muscle cells to constrict, if the endothelium isn't present?
ACh binds to muscarinic receptors on smooth muscle cells -> contraction.
Normally, though, this effect is overwhelmed by the NO produced by endothelial cells in response to ACh.
How does Angiotensin Converting Enzyme (ACE) affect vascular tone? So what if you give an ACE inhibitor?
Bradykinin relaxes vessels.
ACE breaks down bradykinin -> less relaxation.
Angiotensin II (A-2) constricts vessels.
ACE converts A-1 to A-2 -> more constriction.
ACE inhibitors lower blood pressure.
4 factors that cause vasoconstriction?
Angiotensin II (A-2)
ACh (in damaged blood vessels!, eg. atherosclerosis)
Normally people's blood vessels dilate in response to ischemia (such as from blood pressure cuff). But this doesn't happen when there's endothelial dysfunction.
6 risk factors for endothelial dysfunction?
Might high-fat diet induced endothelial dysfunction have something to do with oxidation?
Yeah... (but I don't think taking lots of antioxidants has been shown to increase longevity)
2 instances when you really need angiogenesis to happen? What's one condition where this doesn't work well?
Fracture healing or other wound healing.
Ischemia due to obstruction.
In diabetes, angiogensis is impaired, making these things (and recovery from MI) worse.
What does VEGF act upon to make vessels proliferate?
Endothelial progenitor cells.
What is Hereditary Hemorrhagic Telangectasia (HHT)?
Autosomal dominant condition (defect in Eng or ALK1) that disrupts the control of vessel growth/repair by TGF-beta.
3 consequences of HHT?
Bleeding, esp GI.
Arteriovenous malformations - causing right to left shunting of blood and "paradoxical emboli."
Infection from septic emboli from veins (eg. endocarditis).
2 pro-clot factors mentioned here?
PAI-1 (inhibits t-PA)
A-2 (stimulates PAI-1)
What's Virchow's Triad?
Three factors that make thrombosis likely:
As general, but not absolute rule, are each venous and arterial clots more about fibrin or platelets?
Venous: more about fibrin
Arterial: more about platelets
2 ways in which dysfunctional endothelium leads to a more coagulable state?
Increased vWF -> more platelet aggregation.
Increased PAI-1 -> less t-PA, fibrinolysis.
3 molecules for leukocyte adhesion?
3 inflammation-related / adhesion molecules that A-2 promotes in blood vessels?
Endothelial cells -> VCAM-1 expression
NFkB -> MCP-1
Smooth muscle cells -> IL-6 -> CRP
What adhesion molecule seems to important for bringing immune cells to fat deposits in arteries?
and it's induced by hyperlipidemia
What does turbulent flow have to do with immune cells?
It's easier for immune cells to stick to blood vessel walls when there's turbulent flow.