Lee C M, Cheung W T
Neurosci Lett. 1985 Aug 16;59(1):47-52. doi: 10.1016/0304-3940(85)90213-7.
The inhibitory effects of adenosine as well as its related analogues on the contractile response of the rat vas deferens to field stimulation were compared in the absence and in the presence of nitrobenzylthioguanosine (NBTGR), a potent adenosine uptake inhibitor. In the presence of NBTGR, the order of potency was N6-cyclohexyladenosine (CHA) greater than or equal to L-N6-phenylisopropyladenosine (L-PIA) greater than 2-chloroadenosine greater than D-N6-phenylisopropyladenosine (D-PIA) greater than or equal to adenosine greater than 2'-deoxyadenosine. The inhibitory effect of adenosine but not that of clonidine, beta-endorphin and somatostatin was blocked by 1,3-diethyl-8-phenylxanthine (DPX, pA2 = 7.2), a potent P1-purinergic antagonist. The results suggest that adenosine inhibited the electrically evoked contractions of the rat vas deferens via the activation of the A1 subtype of P1-purinergic receptors.
在不存在和存在强效腺苷摄取抑制剂硝基苄基硫代鸟苷（NBTGR）的情况下，比较了腺苷及其相关类似物对大鼠输精管对场刺激的收缩反应的抑制作用。在NBTGR存在的情况下，效力顺序为N6-环己基腺苷（CHA）≥L-N6-苯基异丙基腺苷（L-PIA）＞2-氯腺苷＞D-N6-苯基异丙基腺苷（D-PIA）≥腺苷＞2'-脱氧腺苷。强效P1-嘌呤能拮抗剂1,3-二乙基-8-苯基黄嘌呤（DPX，pA2 = 7.2）可阻断腺苷的抑制作用，但不阻断可乐定、β-内啡肽和生长抑素的抑制作用。结果表明，腺苷通过激活P1-嘌呤能受体的A1亚型来抑制大鼠输精管的电诱发收缩。
