抑制的行为倍他洛尔在视网膜神经节细胞的离子电流可以解释其神经保护作用。

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Hirooka K,凯利我,Baldridge WH,巴恩斯

抑制的行为倍他洛尔在视网膜神经节细胞的离子电流可以解释其神经保护作用。

Exp眼研究》2000年5月,70(5):611 - 21所示。

PubMed ID

10870519 (在PubMed

]

文摘

倍他洛尔,β1-selective肾上腺素受体拮抗剂,广泛用于治疗青光眼。除了眼降压效果,倍他洛尔被建议作为视网膜神经保护代理(奥斯本et al ., 1997)。调查可能的神经保护作用机制,我们测试了倍他洛尔的行动在离子通道和钙信号在孤立的视网膜神经节细胞。倍他洛尔(50 microM)减少20% high-voltage-activated (HVA)钙通道电流从老虎蝾螈视网膜神经节细胞分离。相比之下,β1-adrenoceptor拮抗剂普萘洛尔(10 microM)和timolol (50 microM)没有抑制行动HVA钙通道电流。l型钙通道拮抗剂,nisoldipine,封锁了HVA钙通道电流部分,剩余电流没有被倍他洛尔。输出电流被抑制在倍他洛尔的存在。iberiotoxin (IBTX;10海里),选择性抑制剂large-conductance Ca-activated K通道,和Cd2 + (100 microM),抑制Ca-activated K通道之后其块Ca渠道,减少输出电流和剩余电流与倍他洛尔不明显阻塞。在倍他洛尔的存在,钠通道电流降低20%左右,随着水流诱发了谷氨酸(10毫米)和GABA(1毫米)。 Current clamp recordings from isolated ganglion cells showed that betaxolol had several effects on excitability: spike height decreased, repetitive spike activity was suppressed, spike width increased and hyperpolarization following spikes was reduced. Calcium imaging in isolated rat retinal ganglion cells revealed that betaxolol inhibited glutamate-induced increases in [Ca2+]i. These results suggest that betaxolol has a diversity of suppressive actions on ganglion cell ion channels and that, as a consequence, one of the net actions of the drug is to reduce Ca2+ influx. The subsequent reduction in [Ca2+]i may contribute to the apparent neuroprotective actions of betaxolol in promoting ganglion cell survival following ischemic insult, as may occur in glaucoma and retinal disease.

DrugBank数据引用了这篇文章

药物靶点

药物	目标	类	生物	药理作用	行动
Timolol	beta 1肾上腺素能受体	蛋白质	人类	是的	拮抗剂	细节