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Caffeine Mechanism of action

caffeine CAS 58--8-2
 

Cas No. [58-08-2]



Caffeine's principal mode of action is as an antagonist of adenosine receptors in the brain.
Caffeine readily crosses the blood–brain barrier that separates the bloodstream from the interior of the brain. Once in the brain, the principal mode of action is as a nonselective antagonist of adenosine receptors. The caffeine molecule is structurally similar to adenosine, and binds to adenosine receptors on the surface of cells without activating them (an "antagonist" mechanism of action). Therefore, caffeine acts as a competitive inhibitor.
Adenosine is found in every part of the body, because it plays a role in the fundamental ATP-related energy metabolism, but it has special functions in the brain. There is a great deal of evidence that concentrations of brain adenosine are increased by various types of metabolic stress including anoxia and ischemia. The evidence also indicates that brain adenosine acts to protect the brain by suppressing neural activity and also by increasing blood flow through A2A and A2B receptors located on vascular smooth muscle. By counteracting adenosine, caffeine reduces resting cerebral blood flow between 22% and 30%. Caffeine also has a generally disinhibitory effect on neural activity. It has not been shown, however, how these effects cause increases in arousal and alertness.
Adenosine is released in the brain through a complex mechanism. There is evidence that adenosine functions as a synaptically released neurotransmitter in some cases, but stress-related adenosine increases appear to be produced mainly by extracellular metabolism of ATP. It is not likely that adenosine is the primary neurotransmitter for any group of neurons, but rather that it is released together with other transmitters by a number of neuron types. Unlike most neurotransmitters, adenosine does not seem to be packaged into vesicles that are released in a voltage-controlled manner, but the possibility of such a mechanism has not been completely ruled out.
Several classes of adenosine receptors have been described, with different anatomical distributions. A1 receptors are widely distributed, and act to inhibit calcium uptake. A2A receptors are heavily concentrated in the basal ganglia, an area that plays a critical role in behavior control, but can be found in other parts of the brain as well, in lower densities. There is evidence that A 2A receptors interact with the dopamine system, which is involved in reward and arousal. (A2A receptors can also be found on arterial walls and blood cell membranes.)
Beyond its general neuroprotective effects, there are reasons to believe that adenosine may be more specifically involved in control of the sleep-wake cycle. Robert McCarley and his colleagues have argued that accumulation of adenosine may be a primary cause of the sensation of sleepiness that follows prolonged mental activity, and that the effects may be mediated both by inhibition of wake-promoting neurons via A1 receptors, and activation of sleep-promoting neurons via indirect effects on A2A receptors. More recent studies have provided additional evidence for the importance of A2A, but not A1, receptors.
Some of the secondary effects of caffeine are probably caused by actions unrelated to adenosine. Like other methylated xanthines, caffeine is both a
1. competitive nonselective phosphodiesterase inhibitor which raises intracellular cAMP, activates PKA, inhibits TNF-alpha and leukotriene synthesis, and reduces inflammation and innate immunity and
2. nonselective adenosine receptor antagonist (see above).
Phosphodiesterase inhibitors inhibit cAMP-phosphodiesterase (cAMP-PDE) enzymes, which convert cyclic AMP (cAMP) in cells to its noncyclic form, thus allowing cAMP to build up in cells. Cyclic AMP participates in activation of protein kinase A (PKA) to begin the phosphorylation of specific enzymes used in glucose synthesis. By blocking its removal caffeine intensifies and prolongs the effects of epinephrine and epinephrine-like drugs such as amphetamine, methamphetamine, or methylphenidate. Increased concentrations of cAMP in parietal cells causes an increased activation of protein kinase A (PKA) which in turn increases activation of H+/K+ ATPase, resulting finally in increased gastric acid secretion by the cell. Cyclic AMP also increases the activity of the funny current, which directly increases heart rate. Caffeine is also a structural analogue of strychnine and like it (though much less potent) a competitive antagonist at ionotropic glycine receptors.
Metabolites of caffeine also contribute to caffeine's effects. Paraxanthine is responsible for an increase in the lipolysis process, which releases glycerol and fatty acids into the blood to be used as a source of fuel by the muscles. Theobromine is a vasodilator that increases the amount of oxygen and nutrient flow to the brain and muscles. Theophylline acts as a smooth muscle relaxant that chiefly affects bronchioles and acts as a chronotrope and inotrope that increases heart rate and efficiency.


Caffeine has a significant effect on spiders, which is reflected in the construction of their webs.



mechanism of action

 

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    Occurrence    
    History    
    Synthesis and properties    
    Pharmacology    
    Metabolism and half-life    
    Mechanism of action >>    
    Effects when taken in moderation    
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    Caffeine intoxication    
    Anxiety and sleep disorders    
    Effects on memory and learning    
    Effects on the heart    
    Effects on children    
    Caffeine intake during pregnancy    
    Decaffeination    
     

caffeine
 

We all know that one of the most powerful chemical compounds found in both coffee and tea is caffeine. Has caffeine become an important part of your daily life? Did you know
Article : What Is Caffeine?

Caffeine is a drug that is naturally produced in the leaves and seeds of many plants. It's also produced artificially and added to certain foods. Caffeine is defined as a drug because it stimulates the central nervous system, causing increased alertness. Caffeine gives most people a temporary energy boost and elevates mood.
Caffeine is in tea, coffee, chocolate, many soft drinks, and pain relievers and other over-the-counter medications. In its natural form, caffeine tastes very bitter. But most caffeinated drinks have gone through enough processing to camouflage the bitter taste.
Teens usually get most of their caffeine from soft drinks and energy drinks. (In addition to caffeine, these also can have added sugar and artificial flavors.) Caffeine is not stored in the body, but you may feel its effects for up to 6 hours.
 


Caffeine Cas No. [58-08-2]


 


 

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