Effects of Adenosine Receptors

摘要: Adenosine, a purine nucleoside catabolite of ATP, regulates numerous effects in mammalian organ systems. The discovery by Drury and Szent-Gyorgy (1929) that adenosine can affect several bodily functions inspired much research interest. Regulatory are especially important when cellular energy supply fails to meet the demand. Adenosine is omnipresent; it released nearly all cells continuously formed intracellularly as well extracellularly. intracellular production mediated an 50-nucleotidase, which dephosphorylates AMP (Schubert et al. 1979; Zimmermann 1998), or hydrolysis S-adenosylhomocysteine (Broch Ueland 1980). It estimated levels interstitial fluid within 30–300 nM range (Winn 1981; Delaney 1998; Geiger Zetterstrom 1982; Porkka-Heiskanen 1997). generated transported into extracellular space via specific bidirectional transporters. through ATP breakdown series ectoenzymes (50-nucleotidase apyrase) (Zimmermann 2000). When high, then inside phosphorylated kinase degraded inosine deaminase (Arch Newsholme 1978; Lloyd Fredholm 1995). increase, up 100-fold, result oxidative stress ischemia (Rudolphi 1992a; Latini al 1999). mediates its activation family four G protein-coupled receptors: A1, A2A, A2B, A3 receptors. All receptors have been cloned from different species. There close similarity between same subtype, at least among mammals, with exception for receptor there almost 30 % difference amino acid level human rat (Fredholm 2000, 2001; Klotz 2000; Zhou 1992). Activation A1 results decreased adenylate cyclase activity proteins Gi/Go family. (VanCalker Londos 1980; Palmer Stiles 1995; Borea 2015). A2A A2B coupled Gs-proteins, both types A2 increases (Palmer Brackett Daly 1994; Peakman Hill 2001, 2011; Sattin Rall 1970; VanCalker 1978). Recently, evidence was presented may be areas (Kull 2000a, b), also activate phospholipase C mast (Feoktistov Biaggioni Besides “canonical” signaling pathways receptors, numbers “noncanonical” each receptor’s described 2000a; Schulte de Lera Ruiz 2014; Chen 2014).