<div>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&lt;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&lt;0.01) and were significantly higher than those in the
capsazepine group (P&lt;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</div>