Decreased secretion of melatonin was reported to be associated with an enhanced risk of hypertension and diabetes. However, the effect of melatonin on gestational hypertension (GH) and the underlying mechanism remain unclear. A GH mouse model was established via electrical stimulation. The hypertensive phenotypes were indicated by systolic blood pressure (SBP) and urinary protein levels. Uterine artery (UtA) endothelial function was detected by relaxation, peak systolic velocity (PSV), end-diastolic velocity (EDV), resistance index (RI) and pulsatility index (PI). Protein expression levels were determined using immunochemistry and Western blots. Pregnancy outcomes were indicated by the fetal live ratio, fetal weight and placental weight. Melatonin supplementation ameliorated hypertensive phenotypes in the mice with GH and enhanced UtA endothelial response to acetylcholine. The BK_Ca potassium channel was involved in the effect of melatonin on UtA endothelial function, and melatonin promoted BK_Ca potassium channel expression and function in UtAs. Finally, melatonin improved pregnancy outcomes in pregnant mice. In conclusion, melatonin ameliorates hypertension in hypertensive pregnant mice and suppresses hypertension-induced decreases in Ca²⁺-activated K⁺ channels in uterine arteries.

据报道，褪黑激素分泌减少与高血压和糖尿病风险增加有关。然而，褪黑激素对妊娠高血压（GH）的影响及其潜在机制仍不清楚。通过电刺激建立GH小鼠模型。高血压表型由收缩压 (SBP) 和尿蛋白水平指示。子宫动脉（UtA）内皮功能通过舒张、收缩期峰值速度（PSV）、舒张末期速度（EDV）、阻力指数（RI）和搏动指数（PI）检测。使用免疫化学和蛋白质印迹测定蛋白质表达水平。妊娠结局由胎儿存活率、胎儿体重和胎盘重量指示。褪黑激素补充剂改善了 GH 小鼠的高血压表型，并增强了 UtA 内皮对乙酰胆碱的反应。BK_Ca钾通道参与了褪黑激素对UtA内皮功能的影响，褪黑激素促进了BK _Ca钾通道在UtA中的表达和功能。最后，褪黑激素改善了怀孕小鼠的妊娠结局。总之，褪黑激素可改善高血压妊娠小鼠的高血压并抑制高血压引起的子宫动脉中 Ca ²⁺激活的 K ^{+通道的减少。}