Objective To explore the role of adenosine A1 receptor (A1R) in pathogenesis of gestational hypertension and preeclampsia. Methods Placenta tissues derived from puerperae with gestational hypertension (n=6), preeclampsia (n=14) and from normal control placentae (n=15) were obtained. The expression location of A1R protein in placenta tissues was detected by immunofluorescence technique, and the expression quantity of A1R protein was performed by Western blotting analysis. We created the normal, hypoxia (8, 24, 48 and 72 h) and hypoxia-reoxygenation trophoblastic cell models, and detected the A1R mRNA and protein expressions in trophoblastic cell models by real-time quantification PCR and Western blotting analysis. Transwell assay was used to determine the invasion ability of trophoblastic cells treated with the A1R antagonist, 8-cyclopentyl-1,3-dipropylxanthine (DPCPX), and Western blotting analysis was used to detect the expression of protein kinase A (PKA) protein. Results We observed that A1R protein was expressed in both trophoblastic cells and vascular endothelial cells. A1R expression was significantly higher in mild and severe preeclampsia placenta tissues than that in normal placenta tissues (P<0.01). A1R expression in the hypoxia model of trophoblast cells significantly was increased with the prolongation of hypoxia (P<0.05). The invasion ability and PKA expression in the hypoxia model of trophoblast cells were significantly lower than those in normal placenta tissues (P<0.01, P<0.05). DPCPX significantly increased the invasion ability of trophoblastic cells and the PKA expression (P<0.05). Conclusion The prolongation of hypoxia can increase the expression of A1R in the trophoblast cells, which may be related to regulated PKA expression.