ArticleInternational journal of molecular sciences2026
Esomeprazole Decreases Soluble Fms-like Tyrosine Kinase-1 in Preeclamptic Pregnancy in Rats.
Article in International journal of molecular sciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Sodium nitrite reduces circulating asymmetric dimethylarginine in a reduced uterine perfusion pressure rat model of preeclampsia.Frontiers in pharmacology · 2026Article
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11 authors.
Funding
Abstract
Preeclampsia is a hypertensive disorder of pregnancy associated with elevated levels of soluble fms-like tyrosine kinase-1 (sFlt-1) and reduced nitric oxide (NO) bioavailability. Esomeprazole (ESO), a proton pump inhibitor (PPI) considered safe during pregnancy, has been proposed to reduce sFlt-1 levels in vitro. This study evaluated the effects of ESO in pregnant rats subjected to reduced uterine perfusion pressure (RUPP), a well-established model of preeclampsia. Pregnant rats received saline (Preg) or ESO (Preg+ESO), while RUPP-operated rats received saline (RUPP) or ESO (RUPP+ESO). At gestational day 21, maternal blood pressure was elevated in the Preg+ESO, RUPP, and RUPP+ESO groups compared with Preg, and ESO did not attenuate RUPP-induced hypertension. Fetal and placental weights were reduced in the RUPP group, whereas ESO increased placental weight in Preg+ESO and RUPP+ESO groups. Gastric pH was elevated by ESO, confirming reduced gastric acidity. Plasma sFlt-1 levels were increased in RUPP and significantly reduced by ESO in RUPP+ESO rats. NO metabolites (NOx) were decreased in RUPP but were unaffected by treatment. Endothelium-dependent relaxation was impaired in the RUPP and RUPP+ESO groups. In conclusion, ESO did not prevent hypertension or endothelial dysfunction, but reduced circulating sFlt-1, suggesting a partial modulatory effect on angiogenic imbalance in experimental preeclampsia.
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