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人类白细胞上的腺苷受体。IV. A1/Ri受体的特性

Adenosine receptors on human leukocytes. IV. Characterization of an A1/Ri receptor.

作者信息

Marone G, Petracca R, Vigorita S, Genovese A, Casolaro V

机构信息

Department of Medicine, University of Naples Federico II, School of Medicine, Italy.

出版信息

Int J Clin Lab Res. 1992;22(4):235-42. doi: 10.1007/BF02591429.

DOI:10.1007/BF02591429
PMID:1334735
Abstract

Adenosine (10(-9)-10(-6) mol/l) and R-phenylisopropyladenosine (10(-9)-10(-7) mol/l) partially inhibited the intracellular accumulation of cyclic AMP induced by isoproterenol, prostaglandin E1, histamine and 5'-N-ethylcarboxamidoadenosine in lymphocytes. In contrast, S-phenylisopropyladenosine, which is a poor agonist of the adenosine A1/Ri receptor, had essentially no inhibitory effect. 8-Phenyltheophylline, in low concentrations that do not inhibit cyclic AMP phosphodiesterase, completely blocked the inhibitory effect of R-phenylisopropyladenosine on the increase in cyclic AMP induced by prostaglandin E1. R-Phenylisopropyladenosine (10(-8)-10(-6) mol/l) also inhibited the cyclic AMP accumulation in lymphocytes induced by forskolin (10(-5) mol/l), which activates adenylate cyclase through direct interaction with the enzyme. We also investigated the presence of the adenosine A1/Ri receptor on human polymorphonuclear leukocytes. R-Phenylisopropyladenosine (3 x 10(-9)-10(-7) mol/l) abolished the stimulating effects of prostaglandin and forskolin on cyclic AMP accumulation in polymorphonuclear leukocytes. This effect was blocked by 8-phenyltheophylline and was not observed with the stereoisomer S-phenylisopropyladenosine. The results support the existence of an A1/Ri receptor that regulates cyclic AMP metabolism of human lymphocytes and polymorphonuclear leukocytes.

摘要

腺苷(10⁻⁹ - 10⁻⁶mol/L)和R-苯异丙基腺苷(10⁻⁹ - 10⁻⁷mol/L)部分抑制了异丙肾上腺素、前列腺素E1、组胺和5'-N-乙基羧酰胺腺苷诱导的淋巴细胞内环磷酸腺苷(cAMP)的细胞内积累。相比之下,作为腺苷A1/Ri受体弱激动剂的S-苯异丙基腺苷基本没有抑制作用。8-苯茶碱在不抑制cAMP磷酸二酯酶的低浓度下,完全阻断了R-苯异丙基腺苷对前列腺素E1诱导的cAMP增加的抑制作用。R-苯异丙基腺苷(10⁻⁸ - 10⁻⁶mol/L)也抑制了福斯高林(10⁻⁵mol/L)诱导的淋巴细胞内cAMP积累,福斯高林通过与该酶直接相互作用激活腺苷酸环化酶。我们还研究了人多形核白细胞上腺苷A1/Ri受体的存在情况。R-苯异丙基腺苷(3×10⁻⁹ - 10⁻⁷mol/L)消除了前列腺素和福斯高林对多形核白细胞内cAMP积累的刺激作用。这种作用被8-苯茶碱阻断,而其立体异构体S-苯异丙基腺苷未观察到这种作用。这些结果支持存在一种调节人淋巴细胞和多形核白细胞cAMP代谢的A1/Ri受体。

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