Objective To investigate the potential mechanism of transient receptor potential vanilloid type 1 (TRPV1) and ATP-sensitive potassium channel (KATP) in severe preeclampsia. Design Basic research. Setting The pathogenesis of severe preeclampsia. Samples Human placental arterioles and HUVECs. Methods (1) Tissue level: The samples were divided into the normotensive pregnancy (NP) group and severe preeclampsia (SP) group. Hematoxylin-eosin staining, quantitative PCR, Western blotting and immunohistochemistry were performed. (2) Cellular level: The samples were divided into the control group, TRPV1 agonist group (capsaicin), and TRPV1 inhibitor group (capsazepine), quantitative PCR and Western blotting were performed. Main Outcome Measures The relative expression of TRPV1, KATP subtype Kir6.1/SUR2B, nitric oxide synthase (eNOS) in placental arterioles ; the relative expression of TRPV1, Kir6.1/SUR2B, and eNOS in the cell groups. Results (1) The endothelial cell layer in the SP group was obviously damaged. The relative gene and protein expression of TRPV1, Kir6.1, SUR2B and eNOS was significantly lower than that in the NP group (P<0.01). (2) The relative gene and protein expression of TRPV1, Kir6.1, SUR2B and eNOS in the control group were significantly lower than those in the capsaicin group (P<0.01) and were significantly higher than those in the capsazepine group (P<0.01). Conclusion TRPV1 plus the downregulation of KATP downregulates the expression of eNOS, reducing vasodilation, which may be critical in the pathogenesis of severe preeclampsia. Funding Luzhou Science and Technology Bureau ( 2020-SYF-27). Key words: Transient receptor potential vanilloid type 1; ATP-sensitive potassium channel; Endothelial nitric oxide synthase; Nitric oxide; Severe preeclampsia