Melatonin ameliorates hypertension in hypertensive pregnant mice and suppresses the hypertension-induced decrease in Ca2+-activated K+ channels in uterine arteries.

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 BKCa potassium channel was involved in the effect of melatonin on UtA endothelial function, and melatonin promoted BKCa 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.