Brownhill V R, Hourani S M, Kitchen I
Receptors and Cellular Regulation Research Group, School of Biological Sciences, University of Surrey, Guildford, UK.
Eur J Pharmacol. 1996 Dec 19;317(2-3):321-8. doi: 10.1016/s0014-2999(96)00721-2.
The ontogeny of P1 purinoceptors in the separated layers of the rat duodenum was investigated using functional assays. In the longitudinal muscle N6-cyclopentyladenosine (CPA) caused relaxations from day 20 that were inhibited by 1,3-dipropyl-8-cyclopentyl-xanthine (DPCPX) (10 nM) indicating an action via adenosine A1 receptors. 5'-N-ethylcarboxamidoadenosine (NECA) caused relaxations at day 15 that were inhibited by DPCPX (1 microM) while 2-p-(2-carboxyethl)phenylethylamino-5'-N-ethylcarboxamidoade nosine (CGS 21680) was almost inactive, indicating an action at adenosine A2B receptors. From day 20 NECA was inhibited by DPCPX (10 nM) but was not antagonised by DPCPX (1 microM) to the extent expected for an adenosine A1 receptor, suggesting activation of adenosine A1 and adenosine A2B receptors. In the muscularis mucosae, CPA and NECA caused contractions from day 10 inhibited by DPCPX (1 microM) while CGS 21680 was less potent, indicating activation of adenosine A2B receptors. These results show that adenosine A2B receptors are present early in the postnatal period, whereas adenosine A1 receptors develop after day 20.
采用功能分析方法研究了大鼠十二指肠各分离层中P1嘌呤受体的个体发生。在纵行肌中，从第20天起，N6-环戊基腺苷（CPA）引起松弛，该松弛被1,3-二丙基-8-环戊基黄嘌呤（DPCPX，10 nM）抑制，表明其通过腺苷A1受体起作用。5'-N-乙基甲酰胺基腺苷（NECA）在第15天引起松弛，该松弛被DPCPX（1 μM）抑制，而2-p-（2-羧乙基）苯乙氨基-5'-N-乙基甲酰胺基腺苷（CGS 21680）几乎无活性，表明其作用于腺苷A2B受体。从第20天起，NECA被DPCPX（10 nM）抑制，但未被DPCPX（1 μM）以腺苷A1受体预期的程度拮抗，提示腺苷A1和腺苷A2B受体均被激活。在黏膜肌层，从第10天起，CPA和NECA引起收缩，该收缩被DPCPX（1 μM）抑制，而CGS 21680的作用较弱，表明腺苷A2B受体被激活。这些结果表明，腺苷A2B受体在出生后早期就已存在，而腺苷A1受体在第20天后发育。
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