BIOL 2420 Lecture Notes - Lecture 6: Thromboxane A2, Secretion, Vasoconstriction
26 Apr 2018
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Unit 3 – Lecture 6
Platelet Activation Begins the Clotting Process
- when a blood vessel wall is first damaged, exposed collagen and chemicals from endothelial cells
activate platelets
- normally
o blood vessels endothelium separates the collagenous matric fibers from the circulating
blood
- when damaged
o collagen is exposed, and platelets rapidly begin to adhere to it
o integrins help platelets adhere to collagen
o integrins are membrane receptor proteins that are linked to the cytoskeleton
▪ binding activates platelets so that they release the contents of their intracellular
granules
• serotonin, ADP, and platelet-activating factor (PAF)
o PAF sets up a positive feedback loop by activating more
platelets
- PAF
o Initiates pathways that convert platelet membrane phospholipids into thromboxane A2
o Serotonin and thromboxane A2 are vasoconstrictors
▪ Also contribute to platelets aggregation, along with ADP and PAF
▪ Net result is a growing platelet plug sealing the damaged vessel
Table 16.4 – factors involved in platelet function
Chemical factor
Source
Activated by or
released in
response to
Role in platelet
plug formation
Other roles and
comments
Collagen
Sub-endothelial
extracellular
matrix
Injury exposes
platelets to
collagen
Binds platelets
to begin
platelet plug
N/A
Von Willebrand
factor (vWF)
Endothelium,
megakaryocytes
Exposure to
collagen
Links platelets
to collagen
Deficiency or defect
causes prolonged
bleeding
Serotonin
Secretory vesicles
of platelets
Platelet
activation
Platelet
aggregation
Vasoconstrictor
Adenosine
diphosphate
(ADP)
Platelet
mitochondria
Platelet
activation,
thrombin
Platelet
aggregation
N/A
Platelet-
activating factor
(PAF)
Platelets,
neutrophils,
monocytes
Platelet
activation
Platelet
aggregation
Plays role in
inflammation; increases
capillary permeability
Thromboxane
A2
Phospholipids in
platelet
membranes
Platelet-
activating factor
Platelet
aggregation
Vasoconstrictor;
eicosanoid
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Document Summary
When a blood vessel wall is first damaged, exposed collagen and chemicals from endothelial cells activate platelets. Normally: blood vessels endothelium separates the collagenous matric fibers from the circulating blood. Initiates pathways that convert platelet membrane phospholipids into thromboxane a2: serotonin and thromboxane a2 are vasoconstrictors, also contribute to platelets aggregation, along with adp and paf, net result is a growing platelet plug sealing the damaged vessel. Table 16. 4 factors involved in platelet function. Promotes wound healing by attracting firboblasts and smooth muscle cells. If platelet aggregation is a positive feedback event, what prevents the platelet plug from continuing to form and spreading beyond the site of injury to other areas of the vessel wall: platelets do not adhere to normal endothelium. Intact vascular endothelial cells convert their membrane lipids into prostacyclin: prostracyclin: an eicosanoid that blocks platelet adhesion and aggregation, nitric oxide released by normal, intact endothelium inhibits platelets from adhering.
