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Introduction
Severe preeclampsia develops as a result of persistent elevated blood pressure and/or urinary protein levels, the progression of maternal organ function or placental‐fetal complications based on preeclampsia[1]. The pathogenesis of this disease has not been fully elucidated. The basic pathophysiological changes are systemic vasospasm and endothelial injury, but the pathogenesis of severe preeclampsia caused by vascular endothelial dysfunction is still unclear[2] . Transient receptor potential vanilloid type 1 (TRPV1) has attracted increasing attention in the study of the cardiovascular system in recent years[3-5] . A recent study showed that dietary capsaicin could activate TRPV1 on endothelial cells and promote the eNOS/NO pathway, which could enhance endothelial production of nitric oxide (NO) and reduce blood pressure in rats with spontaneous hypertension [6] . ATP-sensitive potassium channel (KATP), a specific type of voltage-dependent potassium ion channel, is composed of inwardly rectifying potassium channel (Kir) and sulfonylurea receptor (SUR), and the SUR2B/Kir6.1 subtype is also known as the vascular type [7] . Studies have shown that the KATP channel-specific agonist etakarin not only directly relaxes vascular smooth muscle but also acts on endothelial cells to increase eNOS expression and promote the synthesis and release of NO[8, 9] . At present, correlations between transient receptor potential channels and potassium ion channels have been reported [4, 10, 11] . A study confirmed the involvement of large-conductance K+(BKca) in coronary endothelium-dependent relaxation mediated by TRPV1[4]; however, there have been few reports on TRPV1 and the KATP subtype SUR2B/Kir6.1 in severe preeclampsia. Since the placenta is an important tissue connecting the fetus and the mother and this disease can be rapidly alleviated after delivery of the placenta, the placenta may play an important role in the development of this disease. As one of the vasoactive substances regulating blood flow homeostasis in the body, NO must also be one of the important factors regulating blood flow perfusion in placental arterioles. Therefore, this study aimed to confirm whether severe preeclampsia is caused by impaired expression of TRPV1 and KATP in placental arterioles, leading to impaired eNOS/NO pathway activity, resulting in endothelial dysfunction and decreased diastolic function, and promoting the development of severe preeclampsia.