Lee C M
Neurosci Lett. 1985 Aug 16;59(1):41-5. doi: 10.1016/0304-3940(85)90212-5.
The inhibitory effect of adenosine on the electrically evoked contractions in the rat prostatic vas deferens was markedly dependent on the calcium concentration in the medium, with adenosine being 20 times more potent at lower calcium levels (1.26 mM vs 3.6 mM). Similar calcium dependence of adenosine inhibition was observed in the presence of a potent nucleoside uptake inhibitor, nitrobenzylthioguanosine (NBTGR), suggesting that this calcium dependence of adenosine inhibition was not secondary to an alteration in adenosine uptake. Furthermore, Bay K8644(methyl-1,4-dihydro-2,6- dimethyl-3-nitro-4-(2-trifluoromethylphenyl)pyridine-5-carboxylate), a dihydropyridine 'calcium entry activator', reduced the potency of adenosine in inhibiting the electrically evoked contractions in a calcium-dependent manner. These results support the notion that adenosine might exert its inhibition on neurotransmission in the prostatic rat vas deferens by decreasing transmembrane calcium currents into the nerve terminals and/or the smooth muscles.
腺苷对大鼠前列腺输精管电诱发收缩的抑制作用明显依赖于培养基中的钙浓度，在较低钙水平（1.26 mM对3.6 mM）下，腺苷的效力要强20倍。在存在强效核苷摄取抑制剂硝基苄基硫代鸟苷（NBTGR）的情况下，观察到腺苷抑制的类似钙依赖性，这表明腺苷抑制的这种钙依赖性并非继发于腺苷摄取的改变。此外，二氢吡啶类“钙内流激活剂”Bay K8644（甲基-1,4-二氢-2,6-二甲基-3-硝基-4-（2-三氟甲基苯基）吡啶-5-羧酸酯）以钙依赖性方式降低了腺苷抑制电诱发收缩的效力。这些结果支持这样一种观点，即腺苷可能通过减少进入神经末梢和/或平滑肌的跨膜钙电流来对大鼠前列腺输精管中的神经传递发挥抑制作用。
