Purpose Though the oxygen concentration is 20% in atmosphere, it is around 3% in vivo.Hypoxia is the basic environment in vivo, moderate oxygen concentration can promote cell proliferation.However, if the oxygen concentration is too low or the hypoxia lasts too long, it will cause the cell death.These phenomena are very clear now, but the mechanisms behind them are still unknown.As we all know, HIF-1 α is the main regulator during hypoxia.Our previous experimental results show that hypoxia has an effect on the expression of L-type voltage-dependent Ca2+ channels.In this study, we have focused ofn the regulation of L-type voltage-dependent Ca2+ channels by hypoxia inducible factor-1α (HIF-1α) in hypoxia-enhanced cell death.Methods Detect the effect of HIF-1α inhibitor echinomycin on cell viability with MTS.Detect the expression of L-type voltage-dependent Ca2+ channel subtypes Cav 1.2 and Cav 1.3 by Western blot and real-time PCR methods.Results (1) 3% O2 induced the death of PC 12 cells.(2) After culturing PC 12 cells in 3% O2 and 20% O2 for 24 h with HIF-1 α inhibitor echinomycin in various concentrations, we detected the cell viability with MTS.We found that 1 nM and 5 nM group had an acceptable mortality.(3) Western blot result showed that both Cav1.2 and Cav1.3 proteins were up-regulated during hypoxia, and down-regulated dose-dependently when using HIF-1α inhibitor.(4) PCR data showed that the gene of Cav1.2 has no difference between hypoxia and normoxia treatment, while that of Cav 1.3 increased in hypoxia significantly.Nevertheless, both of them decreased dose-dependently when the culture was treated with the HIF-1α inhibitor.Conclusion Cav1.2/Cav1.3 proteins are correlated positively with HIF-1α in protein level, however, the relationship between Cav1.2/Cav1.3 and HIF-1 α is not very clear in gene level, which needs to be verified further.