In recent years, the prevalence of sleep disturbances during pregnancy has significantly increased due to rising social pressures and lifestyle changes. Studies suggest that circadian rhythm disruption may contribute to blood pressure dysregulation through mechanisms such as hypothalamic-pituitary-adrenal (HPA) axis activation and inflammatory responses. However, the interaction between environmental factors and genetic susceptibility remains unclear. Melatonin receptor 1B (MTNR1B), a key regulator of melatonin signaling, not only modulates circadian rhythms but also plays a critical role in maintaining placental vascular endothelial function. While MTNR1B polymorphisms are strongly associated with type 2 diabetes and insulin resistance, their role in gestational hypertension (GH) susceptibility remains undetermined.

To investigate potential synergistic effects between maternal sleep quality during pregnancy and peripheral blood MTNR1B polymorphisms on GH development.

This study enrolled 235 mid-pregnancy women receiving prenatal care at a provincial hospital in Gansu from March to December 2021, with 235 age-matched healthy pregnant women as controls. Assessments included the Pittsburgh Sleep Quality Index (PSQI), Hospital Anxiety and Depression Scale (HADS), and a pregnancy-specific sleep health questionnaire. Peripheral venous blood was collected before delivery, and improved multiplex ligation detection reaction (im-LDR) technology was employed for genotyping three MTNR1B single-nucleotide polymorphisms (rs3781638, rs10830963, rs3781637). Logistic regression analyzed associations between late-pregnancy sleep parameters, MTNR1B polymorphisms, and GH risk, with multiplicative interaction models evaluating sleep-genotype interactions.

The genotype, allele type, dominant, and over-dominant genotypes comparison of the MTNR1B gene rs3781638 locus in the case group and the control group showed statistically significant differences (P<0.05); there was no statistically significant difference in the comparison of the MTNR1B gene rs10830963 and rs3781637 loci between the two groups (P>0.05). The results of the multivariate Logistics regression analysis showed that carrying the genotype GT (OR=1.88, 95%CI=1.24-2.84), allele type T (OR=1.28, 95%CI=1.02-1.71), dominant genotype GG+GT (OR=1.93, 95%CI=1.29-2.89), and over-dominant genotype GT (OR=1.84, 95%CI=1.22-2.72) were independent risk factors for the occurrence of GH; the interaction analysis results showed that carrying the TT genotype and coughing/snoring 1~2 times/week during nighttime sleep (OR=2.82, 95%CI=1.36-5.84) and coughing/snoring ≥3 times/week (OR=2.21, 95%CI=1.09-4.48) had a significantly higher risk of GH compared to carrying the TT genotype and no coughing/snoring during nighttime sleep (P<0.05); compared to carrying the TT genotype and no coughing/snoring during nighttime sleep, carrying the GT+GG genotype, regardless of coughing/snoring during nighttime sleep, increased the risk of GH, with the highest risk of GH occurring when coughing/snoring ≥3 times/week (OR=4.90, 95%CI=2.24-10.75).

The MTNR1B rs3781638 (G>T) polymorphism may confer GH susceptibility and demonstrate synergistic effects with nocturnal snoring on GH pathogenesis.