Text
Introduction
Severe preeclampsia develops as a result of persistent elevated blood
pressure and/or urinary protein levels, the progression of maternal
organ function or placentalāfetal 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.