ArticleCellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology2018
In Utero Exposure to Fine Particulate Matter Causes Hypertension Due to Impaired Renal Dopamine D1 Receptor in Offspring.
Article in Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 32 citations in OpenAlex.
- Prenatal air pollution exposure and placental vasculature development among participants of the UPSIDE cohort study.Environmental research · 2025Article
- Gestational exposure to micro and nanoplastics differentially impacts cardiac development and function in male and female rats throughout the lifespan.Toxicology and applied pharmacology · 2025Article
- Environmental Nephrotoxicity Across the Life Course: Oxidative Stress Mechanisms and Opportunities for Early Intervention.Antioxidants (Basel, Switzerland) · 2025Review
- Renal glomerular and tubular injury in the offspring of the preeclampsia-like syndrome.Scientific reports · 2025Article
- G protein-coupled receptor kinases in hypertension: physiology, pathogenesis, and therapeutic targets.Hypertension research : official journal of the Japanese Society of Hypertension · 2024Review
- The Impact of the Aryl Hydrocarbon Receptor on Antenatal Chemical Exposure-Induced Cardiovascular-Kidney-Metabolic Programming.International journal of molecular sciences · 2024Review
- Toxicological Effects of Fine Particulate Matter (PMWater, air, and soil pollution · 2023Review
- Comprehensive insights in GRK4 and hypertension: From mechanisms to potential therapeutics.Pharmacology & therapeutics · 2022Review
- The Physiological Effects of Air Pollution: Particulate Matter, Physiology and Disease.Frontiers in public health · 2022Review
- Paternal long-term PM2.5 exposure causes hypertension via increased renal AT1R expression and function in male offspring.Clinical science (London, England : 1979) · 2021Article
- Air pollution and children's health-a review of adverse effects associated with prenatal exposure from fine to ultrafine particulate matter.Environmental health and preventive medicine · 2021Review
- Particulate Matter, an Intrauterine Toxin Affecting Foetal Development and Beyond.Antioxidants (Basel, Switzerland) · 2021Article
- Renal Dopamine Receptors and Oxidative Stress: Role in Hypertension.Antioxidants & redox signaling · 2021Review
- The Role of the Renal Dopaminergic System and Oxidative Stress in the Pathogenesis of Hypertension.Biomedicines · 2021Review
- Adverse Impact of Environmental Chemicals on Developmental Origins of Kidney Disease and Hypertension.Frontiers in endocrinology · 2021Review
- Prenatal Exposure toEnvironmental health perspectives · 2019Article
- Prenatal cold exposure causes hypertension in offspring by hyperactivity of the sympathetic nervous system.Clinical science (London, England : 1979) · 2019Article
- Role of Thioredoxin 1 in Impaired Renal Sodium Excretion of hDJournal of the American Heart Association · 2019Article
- Long-term low salt diet increases blood pressure by activation of the renin-angiotensin and sympathetic nervous systems.Clinical and experimental hypertension (New York, N.Y. : 1993) · 2019Article
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Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
Abstract
BACKGROUND/
aimsAdverse environment in utero can modulate adult phenotypes including blood pressure. Fine particulate matter (PM2.5) exposure in utero causes hypertension in the offspring, but the exact mechanisms are not clear. Renal dopamine D1 receptor (D1R), regulated by G protein-coupled receptor kinase type 4 (GRK4), plays an important role in the regulation of renal sodium transport and blood pressure. In this present study, we determined if renal D1R dysfunction is involved in PM2.5-induced hypertension in the offspring.
methodsPregnant Sprague-Dawley rats were given an oropharyngeal drip of PM2.5 (1.0 mg/kg) at gestation day 8, 10, and 12. The blood pressure, 24-hour sodium excretion, and urine volume were measured in the offspring. The expression levels of GRK4 and D1R were determined by immunoblotting. The phosphorylation of D1R was investigated using immunoprecipitation. Plasma malondialdehyde and superoxide dismutase levels were also measured in the offspring.
resultsAs compared with saline-treated dams, offspring of PM2.5-treated dams had increased blood pressure, impaired sodium excretion, and reduced D1R-mediated natriuresis and diuresis, accompanied by decreased renal D1R expression and GRK4 expression. The impaired renal D1R function and increased GRK4 expression could be caused by increased reactive oxidative stress (ROS) induced by PM2.5 exposure. Administration of tempol, a redox-cycling nitroxide, for 4 weeks in the offspring of PM2.5-treated dam normalized the decreased renal D1R expression and increased renal D1R phosphorylation and GRK4 expression. Furthermore, tempol normalized the increased renal expression of c-Myc, a transcription factor that regulates GRK4 expression.
conclusionsIn utero exposure to PM2.5 increases ROS and GRK4 expression, impairs D1R-mediated sodium excretion, and increases blood pressure in the offspring. These studies suggest that normalization of D1R function may be a target for the prevention and treatment of the hypertension in offspring of mothers exposed to PM2.5 during pregnancy.
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