ReviewPharmacological characterization of novel A3 adenosine receptor-selective antagonists
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2018, Bioorganic and Medicinal Chemistry LettersP2Y<inf>13</inf> receptors mediate presynaptic inhibition of acetylcholine release induced by adenine nucleotides at the mouse neuromuscular junction
2016, NeuroscienceCitation Excerpt :On the other hand, IDP might be metabolized into inosine, which we demonstrated is able to activate A3 adenosine receptors and decrease spontaneous and evoked ACh release at mammalian MNJs (Cinalli et al., 2013). So, to rule out the possibility that IDP may exert its inhibitory effect through its metabolite inosine, we studied its action in the presence of the specific A3 receptor antagonist MRS-1191 (5 μM; Jiang et al., 1996; Jacobson et al., 1997). In these conditions, the effect of 100 μM IDP upon MEPP frequency remained unchanged (MRS-1191 99.5 ± 0.7% of control values, MRS-1191 + IDP 59.1 ± 1.5%, n = 3, P < 0.001, Fig. 3C), suggesting that IDP modulates spontaneous secretion by activating P2Y13 receptors.
ATP releases ATP or other nucleotides from human peripheral blood leukocytes through purinergic P2 receptors
2016, Life SciencesCitation Excerpt :We chose this relatively low concentration of ATPγS because at higher concentrations, it causes cell death [35]. Finally, in another set of experiments, a mixture of MNC + PMN cells were pre-incubated with or without 100 nM 8-cyclopentyl-1,3-dipropylxanthine (DPCPX, an antagonist of A1 receptors [36]), 10 μM MRS 1191 (an antagonist of A3 receptors [37]), 100 nM SCH-58261 (SCH, an antagonist of A2A receptors [38]), or 10 μM MRS 1754 (an antagonist of A2B receptors [39]). All the antagonist or inhibitor drugs were pre-incubated during 10 min before ATP, UTP, or ATPγS addition.