Li J P, Edward D P, Lam T T, Tso M O
Department of Ophthalmology, University of Illinois, Chicago College of Medicine 60612.
Res Commun Chem Pathol Pharmacol. 1991 Jun;72(3):347-52.
A recent study demonstrated the amelioration of light-induced photoreceptor degeneration by flunarizine and suggested that the protective effect achieved by the drug may be due to the inhibition of inositol 1,4,5-trisphosphate-induced calcium release from intracellular stores or the inhibition of calcium entry through putative voltage-sensitive calcium channels. In the current study, we investigated the effect of nimodipine, a specific voltage-sensitive calcium channel blocker, in light-induced retinal degeneration to further define the factors involved in the retinal degenerative process. Morphological, morphometric, and biochemical results demonstrated that nimodipine was ineffective in ameliorating light-induced retinal degeneration, and implied that calcium entry through voltage-sensitive channels is unlikely to be involved in this disease process, and inositol 1,4,5-trisphosphate-induced calcium release from intracellular stores may play a dominant role in light-induced photoreceptor cell damage.
最近的一项研究证明了氟桂利嗪可改善光诱导的光感受器变性,并表明该药物所实现的保护作用可能是由于抑制了肌醇1,4,5-三磷酸诱导的细胞内钙库钙释放,或抑制了通过假定的电压敏感性钙通道的钙内流。在本研究中,我们研究了特异性电压敏感性钙通道阻滞剂尼莫地平在光诱导的视网膜变性中的作用,以进一步明确参与视网膜变性过程的因素。形态学、形态计量学和生化结果表明,尼莫地平在改善光诱导的视网膜变性方面无效,这意味着通过电压敏感性通道的钙内流不太可能参与该疾病过程,且肌醇1,4,5-三磷酸诱导的细胞内钙库钙释放可能在光诱导的光感受器细胞损伤中起主要作用。