Aim: This study aimed to investigate the effects of relaxin (RLX) on hypertensive disorders of pregnancy (HDP) and fetal growth restriction (FGR) using a nitric oxide synthase (NOS) inhibitor-induced HDP murine model.

Methods: Pregnant C57BL/6NCrSlc mice were divided into three groups at 6 days post coitum (dpc). The control group (control) received saline by subcutaneous injection at 6–10 dpc. The NOS inhibitor group (L-NAME) received 50 mg/kg/day L-NG-nitro arginine methyl ester (L-NAME) by subcutaneous injection at 6–10 dpc. The RLX combination group (L-NAME+RLX) received the same dose of L-NAME plus 0.5 μg/g/day human relaxin-2 by subcutaneous injection at 6–10 dpc. Maternal systolic blood pressure (SBP) and urinary protein were assessed at 16 dpc. At 17 dpc, fetal weight was recorded, and placentas, maternal serum, and kidneys were collected.

Results: Maternal SBP and fetal weight were improved in L-NAME+RLX mice compared with L-NAME mice. No significant differences were observed in abortion rate, urinary protein, placental weight, serum placental growth factor concentration, and glomerular open capillary area.

Conclusion: RLX improved maternal SBP and FGR, suggesting that RLX may be a candidate drug for prophylaxis of HDP with FGR.

We present the case of a 40-year-old woman who experienced severe hypertension during her first pregnancy. Hypertension persisted after delivery, prompting admission to the Department of Endocrinology and Metabolism at our hospital. Examination revealed an aldosterone-producing adenoma, and she was diagnosed with primary aldosteronism. Her hypertension was controlled using methyldopa. She became pregnant again in April 2019, and in the ninth week of pregnancy, she underwent her first medical examination of the artery. Subsequently, the methyldopa dose was increased to control her hypertension. However, her hypertension worsened, and she tested positive for urinary albumin, prompting hospital admission at 32 weeks of gestation. Her oral medication was changed to nifedipine, which was continued after her second delivery. However, her hypertension persisted. Therefore, a selective mineralocorticoid receptor antagonist was administered, and her hypertension improved. Mineralocorticoid receptor antagonists should be considered when blood pressure is poorly controlled owing to worsening primary aldosteronism.

A 23-year-old woman (gravida 3, para 2) was referred to our hospital at 29 weeks of gestation by a nearby doctor due to hydramnios and suspected umbilical cord hernia. Ultrasound and magnetic resonance imaging indicated hydramnios, umbilical cord hernia, and a dilated stomach, with suspicion of upper gastrointestinal atresia. She was hospitalized at 33 weeks of gestation owing to membrane rupture. Fetal bradycardia was observed during delivery, and an emergency cesarean section was performed. A female infant weighing 1,799 g was delivered (Apgar score: 1/1); hemorrhagic ulceration of the umbilical cord was observed. Pancreatic phospholipase A2, trypsin, lipase, and bile acid levels in the amniotic fluid were elevated. The infant died of hemorrhagic shock and circulatory failure on the second day after birth. Based on these findings, we hypothesize that umbilical cord ulceration or hemorrhage may occur in congenital upper gastrointestinal atresia due to discharge of fetal gastrointestinal enzymes into the amniotic fluid.