Adenosine receptors calcium mobilization

Three major mechanisms of action have dominated as possible explanations for the ergogenic potential of caffeine in the enhancement of exercise performance. These three mechanisms involve (1) the mobilization of intracellular calcium from the sarcoplasmic reticulum of skeletal muscle, (2) the increase of cyclic-3 ,5 -adenosine monophosphate (cAMP) by the inhibition of phosphodiesterases in muscles and adipocytes, and (3) the competitive antagonism of adenosine receptors, primarily in the central nervous system (CNS).8 9... 

Rail, T. W., Evolution of the mechanism of action of methylxanthines From calcium mobilizers to antagonists of adenosine receptors, Pharmacologist, 24, 277, 1982. 

Although caffeine is known to mobilize intracellular calcium, to inhibit phosphodiesterase activity, and to increase in vitro 5-HT and NE concentrations in the brainstem (Garrett and Griffiths 1997 Berkowitz et al. 1970 Carter et al. 1995 Solinas et al. 2002), it is now widely accepted that the mechanism of action of caffeine on wakefulness, at least at the dose range produced by voluntary caffeine intake, is via the antagonism of adenosine receptors. 

There are three important ADP receptors on the platelet surface. The P2X, is related with the rapid influx of calcium into the cytosol the P2Y1 mediates mobilization of calcium through activation of phospholipase C and shape change, and the P2Y12 receptor is coupled to adenyl cyclase inhibition mediated by a G-protein with subsequent decrease of the cyclic adenosine monophosphate (cAMP). The decrease of cAMP stimulates dephosphorylation of vasodilator-stimulated phosphoprotein that is closely correlated with the GPIIb/llla activation. Thienopyridines compounds promote platelet inhibition mainly by blocking the P2Y12 receptor. 

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