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Titlebook: Cardiovascular Biology of Purines; Geoffrey Burnstock,James G. Dobson,Joel Linden Book 1998 Springer Science+Business Media New York 1998

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https://doi.org/10.1007/978-1-349-05984-3bit transmitter release via prejunctional A. receptors thereby diminishing α. adrenoceptor-mediated vasoconstriction. Presumably, not only adenosine but also ATP inhibits transmitter release through activation of presynaptic A. receptors which might explain various observations previously ascribed t
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Adenosine Receptor Subtypes and Cardioprotection in Cardiac Myocyte and Transgenic Models, or “primes” K. channels. The primed channels can be more responsive to adenosine released during the ischemia and thus protect the myocytes. Although unproven, evidence is growing to support this sequence of signaling events in mediating the protective effect of ischemie preconditioning. Activation
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Molecular Biology of P2X Purinoceptors,terms of receptor stoichiometry, the lining of the ion pore, means by which the ionchannel opens and closes, allosteric modulatory sites, the ligand docking site and reasons for selectivity of nucleotidic analogues. The situation has been compounded by the discovery of splice variants of P2X subunit
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The G Protein-Coupled P2Y Receptors, pharmacological responses of various tissues with a specific receptor. The most encouraging progress in drug development has been in the synthesis of selective agonists and antagonists for the P2Y. receptor. Mutational and modeling analyses have provided some insight into identification of the bind
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P2-Purinoceptors and Cardiac Functions,recombinant receptors specific for ATP divided in two families cf ionotropic ligand-gated ion channels P2X-purinoceptors and metabotropic G protein-coupled P2Y-purinoceptors. Molecular characterization and localization of several P2-purinoceptor subtypes in the heart provide functional evidence in f
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