Activation and Desensitization of Rat A(3)-Adenosine Receptors by Selective Adenosine Derivatives and Xanthine-7-Ribosides

选择性腺苷衍生物和黄嘌呤-7-核苷对大鼠A(3)-腺苷受体的激活和脱敏作用

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Abstract

Strategy, Management and Health PolicyVenture Capital Enabling TechnologyPreclinical ResearchPreclinical Development Toxicology, Formulation Drug Delivery, PharmacokineticsClinical Development Phases I-III Regulatory, Quality, ManufacturingPostmarketing Phase IV Xanthine and adenosine derivatives, known to bind to recombinant rat A(3) adenosine receptors stably expressed in Chinese hamster ovary cells, were characterized in a functional assay consisting of activation of A(3) receptor-stimulated binding of [(35)S]GTPγS in rat RBL-2H3 cell membranes. 1,3-Dibutylxanthine-7-riboside-5'-N-methylcarboxamide (DBXRM, 7b), previously shown to inhibit adenylyl cyclase via rat A(3) receptors with full efficacy, appeared to be a partial agonist at the rat A(3) receptor of RBL-2H3 cells. Full agonists, such as Cl-IB-MECA or I-AB-MECA, were more potent and effective than the partial agonist DBXRM in causing desensitization of rat A(3) receptors, as indicated by loss of [(35)S]GTPγS binding. At A(1) receptors, antagonism of agonist-elicited inhibition of rat adipocyte adenylyl cyclase was observed for several xanthine-7-riboside derivatives that had been shown to be full agonists at rat A(3) receptors. A new xanthine riboside (3'-deoxyDBXRM, 7c) was synthesized and found to be a partial agonist at rat A(3) receptors and an antagonist at rat A(1) receptors. Thus, it is possible for the same compound to stimulate one adenosine receptor subtype (A(3)) and block another subtype (A(1)) within the same species.

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