wyb
Forum Junior
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Aspirin blocks cycloxygenase in arachidonic acid metabolism, but why is the cycloxygenase of platelet vs endothelial cell react differently to Aspirin?  Thanks alot!
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| sergey1987apr
Forum Newbie
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Aspiring blocks cyclooxygenase
And through blocking cyclo-oxygenase, it blocks synthesis of thromboxane A2 and hence inhibits platelet aggregation
For the effect on GI tract, analgesic, anti-pyretic effect, it blocks cyclo-oxygenase too and decrease PGE.
I think it's the same - inhibition of cyclo-oxygenase?
sorry if im wrong...
my knowledge is very limited 
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| sergey1987apr
Forum Newbie
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typing mistake sorry "aspirin" not "aspiring"...
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| new_n_lost
Politically InCorrect
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Good Question and a very interesting Concept.
Cyclo-oxygenase is in 2 isoforms in the body. COX 1 and 2. COX-1 is the isoform normally present in many tissues associated with the production of prostanoids for physiological functions, whereas COX-2 is the inducible isoform that appears at sites of inflammation and is associated with the production of prostanoids involved in inflammatory responses.
Now COX products are that important to the normal functioning of the cardiovascular system, particularly prostaglandin (PG) I2 produced by endothelial cells and thromboxane (Tx) A2 formed by platelets. PGI2 is antithrombotic and vasodilating; it also reduces vascular remodeling and limits cholesterol uptake. In contrast, TxA2 is prothrombotic and vasoconstricting, and promotes vascular remodeling. Drugs that inhibit TxA2 production therefore reduce platelet reactivity whereas drugs that inhibit PGI2 production increase it. In clinical use, low-dose aspirin works by inhibiting COX in platelets and reducing TxA2 production while having relatively less effect on PGI2 production.
So it can be concluded that the platelet and endothelial cell COX has a different response to Aspirin. Plus there are some studies which suggest that COX 2 isoform only appears when there is mechanical forces are involved such as in lumens of blood vessels.
Hope this helps.
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| new_n_lost
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http://archinte.ama-assn.org/cgi/content/full/160... <<< The best article so far i have found this and a very very interesting one.
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FORUM RULES-- Those who believe in telekinesis, raise my hand. I get enough exercise just by pushing my luck --P4U World.." The pure and simple truth is rarely pure and never simple."
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| pr20
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Thanks for the great work n_n_l
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| 1.ammara
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well, i was just to mention the other effects of COX-2, but this above mentioned article has beautifully elaborated them, thats nice!
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| wyb
Forum Junior
Topics: 8
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To sergey1987, thanks alot! you'r right, it depends on the dosage of Aspirin.
To new_n_lost, thank you for the detail explanation and the lately paper! It is so good that it instructs me to know more about COX1 and COX2.
"Aspirin's ability to suppress the production of prostaglandins and thromboxanes is due to its competitive and irreversible inactivation of the COX enzyme. 40 mg of aspirin a day is able to inhibit a large proportion of maximum thromboxane A2 ( induced by COX1)release provoked acutely, with the PGI2 synthesis (stimulated by COX2) being little affected; however, higher doses of aspirin are required to attain further inhibition."
That is very nice!
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