Cheung W T, Shi M M, Young J D, Lee C M
Biochem Pharmacol. 1987 Jul 1;36(13):2183-6. doi: 10.1016/0006-2952(87)90148-1.
Two dihydropyridine compounds, Bay K8644 (a calcium entry activator) and nifedipine (a calcium entry blocker), were found to inhibit the binding of [3H]phenylisopropyladenosine ([3H]PIA) to A1 adenosine receptors in rat cerebral cortex membranes with comparable potencies (IC50 10-30 microM). Scatchard analyses indicated that both Bay K8644 and nifedipine inhibited the binding of [3H]PIA by increasing the KD but without significant effect on the Bmax. When tested at 100 microM, neither Bay K8644 nor nifedipine showed a significant effect on [3H]-p-aminoclonidine ([3H]PAC; alpha 2-adrenergic receptor), [3H]dihydroalprenolol ([3H]DHA; beta-adrenergic receptor), [3H]spiperone (dopamine receptor), and [3H]nitrobenzylthioinosine [( 3H]NBMPR; nucleoside transporter) binding. In the presence of 10 mM Mg2+, the ability of 2-chloroadenosine (2-Cl-Ad, an A1 adenosine receptor agonist) to displace [3H]PIA binding was increased. Conversely, the potencies of 1,3-diethyl-8-phenylxanthine (DPX; an A1 receptor antagonist), Bay K8644 and nifedipine in inhibiting [3H]PIA binding were unchanged. It is suggested that both Bay K8644 and nifedipine may act as antagonists of adenosine A1 receptors, in addition to their well-known effects on calcium channels.
发现两种二氢吡啶化合物，即Bay K8644（一种钙内流激活剂）和硝苯地平（一种钙内流阻滞剂），能以相当的效力（IC50为10 - 30微摩尔）抑制[3H]苯基异丙基腺苷（[3H]PIA）与大鼠大脑皮层膜中A1腺苷受体的结合。Scatchard分析表明，Bay K8644和硝苯地平均通过增加解离常数（KD）来抑制[3H]PIA的结合，但对最大结合容量（Bmax）无显著影响。当以100微摩尔进行测试时，Bay K8644和硝苯地平对[3H]-对氨基可乐定（[3H]PAC；α2 - 肾上腺素能受体）、[3H]二氢阿普洛尔（[3H]DHA；β - 肾上腺素能受体）、[3H]螺哌隆（多巴胺受体）和[3H]硝基苄基硫代肌苷（[3H]NBMPR；核苷转运体）的结合均无显著影响。在10毫摩尔镁离子存在的情况下，2 - 氯腺苷（2 - Cl - Ad，一种A1腺苷受体激动剂）置换[3H]PIA结合的能力增强。相反，1,3 - 二乙基 - 8 - 苯基黄嘌呤（DPX；一种A1受体拮抗剂）、Bay K8644和硝苯地平抑制[3H]PIA结合的效力未改变。提示Bay K8644和硝苯地平除了对钙通道有众所周知的作用外，可能还作为腺苷A1受体的拮抗剂发挥作用。
