Nektar
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This is some info i have aranged on the mechanism through which Caffeine can increase prostaglandin production from ArA. I was wondering what you guys think of this unusual effect of a substance that is known to be a vasoconstrictor being an anabolic, vasodilator?
Directly: ^Caffeine --> ^epinephrine --> ^cAMP --> Body responds with ^phosphodiesterase and ^prostaglandins to lower cAMP levels --> PUMPS!
Indirectly: ^Caffeine --> inhibits phosphodiesterase production (but doesn’t reduce prostaglandins) --> sustains elevated cAMP levels --> PUMPS!
Also: Norepinephrine activates NO synthase --> ^production of NO --> activates cyclooxygenase --> ^production of PGE2
However, in the absence of norepinephrine it is beleived that NO synthase is not activated because of low intracellular calcium.
Solution?: Caffeine --> ^Ca++ release from the sarcoplasmic reticulum --> ^intracellular Ca++ --> activates phospholipase A2
and
Caffeine --> ^in myofribrilar Ca++ sensitivity
Therefore Caffeine --> norepinephrine --> activates arachidonic acid release, which is then converted into PGE2 by the NO-induced activation of cyclooxygenase. Is this correct? please feel free to help evaluate the effectiveness of ArA with caffeine. Thanks!
Also, here's something about insulin increasing not only ArA's conversion to PGs:
source:
cant post links yet so search [Prostaglandins and nitric oxide mediate insulin-induced vasodilation in the human forearm]
Directly: ^Caffeine --> ^epinephrine --> ^cAMP --> Body responds with ^phosphodiesterase and ^prostaglandins to lower cAMP levels --> PUMPS!
Indirectly: ^Caffeine --> inhibits phosphodiesterase production (but doesn’t reduce prostaglandins) --> sustains elevated cAMP levels --> PUMPS!
Also: Norepinephrine activates NO synthase --> ^production of NO --> activates cyclooxygenase --> ^production of PGE2
However, in the absence of norepinephrine it is beleived that NO synthase is not activated because of low intracellular calcium.
Solution?: Caffeine --> ^Ca++ release from the sarcoplasmic reticulum --> ^intracellular Ca++ --> activates phospholipase A2
and
Caffeine --> ^in myofribrilar Ca++ sensitivity
Therefore Caffeine --> norepinephrine --> activates arachidonic acid release, which is then converted into PGE2 by the NO-induced activation of cyclooxygenase. Is this correct? please feel free to help evaluate the effectiveness of ArA with caffeine. Thanks!
Also, here's something about insulin increasing not only ArA's conversion to PGs:
source:
cant post links yet so search [Prostaglandins and nitric oxide mediate insulin-induced vasodilation in the human forearm]