ArticleFree radical biology & medicine2014
Prenatal lipopolysaccharide exposure results in dysfunction of the renal dopamine D1 receptor in offspring.
Article in Free radical biology & medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 30 citations in OpenAlex.
- The roles of G protein-coupled receptor kinase 2 in renal diseases.Journal of cellular and molecular medicine · 2024Review
- G protein-coupled receptor kinases in hypertension: physiology, pathogenesis, and therapeutic targets.Hypertension research : official journal of the Japanese Society of Hypertension · 2024Review
- Dopamine, Immunity, and Disease.Pharmacological reviews · 2023Review
- Comprehensive insights in GRK4 and hypertension: From mechanisms to potential therapeutics.Pharmacology & therapeutics · 2022Review
- Prenatal Lipopolysaccharides Exposure Induces Transgenerational Inheritance of Hypertension.Circulation · 2022Article
- Renal Dopamine Receptors and Oxidative Stress: Role in Hypertension.Antioxidants & redox signaling · 2021Review
- Maternal inflammation exacerbates neonatal hyperoxia-induced kidney injury in rat offspring.Pediatric research · 2019Article
- Prenatal cold exposure causes hypertension in offspring by hyperactivity of the sympathetic nervous system.Clinical science (London, England : 1979) · 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
- Long-Term Exposure of Fine Particulate Matter Causes Hypertension by Impaired Renal DJournal of the American Heart Association · 2018Article
- In Utero Exposure to Fine Particulate Matter Causes Hypertension Due to Impaired Renal Dopamine D1 Receptor in Offspring.Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2018Article
- Primary Pediatric Hypertension: Current Understanding and Emerging Concepts.Current hypertension reports · 2017Review
- Ascorbic Acid Protects against Hypertension through Downregulation of ACE1 Gene Expression Mediated by Histone Deacetylation in Prenatal Inflammation-Induced Offspring.Scientific reports · 2016Article
- G Protein-Coupled Receptor Kinases: Crucial Regulators of Blood Pressure.Journal of the American Heart Association · 2016Review
- Post-Natal Inhibition of NF-κB Activation Prevents Renal Damage Caused by Prenatal LPS Exposure.PloS one · 2016Article
- Co-occurrence of preconception maternal childhood adversity and opioid use during pregnancy: Implications for offspring brain development.Neurotoxicology and teratologyArticle
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
Abstract
Adverse environment in early life can modulate the adult phenotype, including blood pressure. Lipopolysaccharide (LPS) exposure in utero results in increased blood pressure in the offspring, but the exact mechanisms are not clear. Studies have shown that the renal dopamine D1 receptor (D1R) plays an important role in maintaining sodium homeostasis and normal blood pressure; dysfunction of D1R is associated with oxidative stress and hypertension. In this study, we determined if dysfunction of the renal D1R is involved in fetal-programmed hypertension, and if oxidative stress contributes to this process. Pregnant Sprague-Dawley (SD) rats were intraperitoneally injected with LPS (0.79 mg/kg) or saline at gestation days 8, 10, and 12. As compared with saline-injected (control) dams, offspring of LPS-treated dams had increased blood pressure, decreased renal sodium excretion, and increased markers of oxidative stress. In addition, offspring of LPS-treated dams had decreased renal D1R expression, increased D1R phosphorylation, and G protein-coupled receptor kinase type 2 (GRK2) and type 4 (GRK4) protein expression, and impaired D1R-mediated natriuresis and diuresis. All of the findings in the offspring of LPS-treated dams were normalized after treatment with TEMPOL, an oxygen free radical scavenger. In conclusion, prenatal LPS exposure, via an increase in oxidative stress, impairs renal D1R function and leads to hypertension in the offspring. Normalization of renal D1R function by amelioration of oxidative stress may be a therapeutic target of fetal programming of hypertension.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.