To investigate the mechanism of sphingosine-1-phosphate (S1P) in contraction of human aortic vascular smooth muscle cells (T/G HA-VSMC) under hypoxic/ischemic stress. Methods: The cultured T/ G HA-VSMC were divided into normal control group and ischemia-hypoxia model group. In the ischemia-hypoxia group, T/G HA-VSMC cells were cultured under hypoxic conditions to simulate the ischemic-hypoxic environment induced by subarachnoid hemorrhage (SAH). The mRNA expression of sphingosine kinase 1 (SphK1) was detected by QT-PCR, and the protein levels of SphK1 were measured by western blot. The levels of S1P in the supernatant of the cell culture medium were measured by ELISA. Lentivirus vector shRNA mediated SphK1 gene silencing was applied as a reverse study. The calcium fluorescent probe Fluo-3/AM was used to measure intracellular Ca2 + concentration. Results: Compared with that of normal control group, the protein expression of SphK1 in T/G HA-VSMC was significantly increased in the ischemia-hypoxia group, and the concentration of S1P in the supernatant of the cell culture medium was increased significantly in the ischemia-hypoxia group. The concentration of intracellular Ca2+ increased significantly in T/G HA-VSMC under ischemia and hypoxia stress, and exogenous S1P significantly increased the intracellular Ca2 + concentration. Compared with normal control group, shRNA interference SphK1 gene expression and SphK1 specific inhibitors dimethylsphingosine (DMS) significantly inhibited the concentrations of both S1P and Ca2+ in T/G HA-VSMC in the ischemia-hypoxia group. Conclusion: SphK1 gene expression is up-regulated in T/G HA-VSMC cells under ischemic/hypoxic stress, which promotes the synthesis and metabolism of S1P. High concentration of S1P leads to vasoconstriction by increasing the level of intracellular Ca2+ in cells.