ArticleActa pharmacologica Sinica2014
PPARα ligand clofibrate ameliorates blood pressure and vascular reactivity in spontaneously hypertensive rats.
Article in Acta pharmacologica Sinica, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 17 citations in OpenAlex.
- Parental diet and offspring health: a role for the gut microbiome via epigenetics.Nature reviews. Gastroenterology & hepatology · 2025Review
- Kidney Programming and Hypertension: Linking Prenatal Development to Adulthood.International journal of molecular sciences · 2024Review
- Oxidative Stress in Kidney Injury and Hypertension.Antioxidants (Basel, Switzerland) · 2024Review
- An insight to treat cardiovascular diseases through phytochemicals targeting PPAR-α.Molecular and cellular biochemistry · 2024Review
- Review
- Clofibrate, a Peroxisome Proliferator-Activated Receptor-Alpha (PPARα) Agonist, and Its Molecular Mechanisms of Action against Sodium Fluoride-Induced Toxicity.Biological trace element research · 2022Article
- Animal Models for DOHaD Research: Focus on Hypertension of Developmental Origins.Biomedicines · 2021Review
- Role of the Peroxisome Proliferator Activated Receptors in Hypertension.Circulation research · 2021Review
- Effect of berberine on PPARPharmaceutical biology · 2017Article
- Functional Regression Models for Epistasis Analysis of Multiple Quantitative Traits.PLoS genetics · 2016Article
- Comparative transcriptional profiling of renal cortex in rats with inherited stress-induced arterial hypertension and normotensive Wistar Albino Glaxo rats.BMC genetics · 2016Article
- PPARs Link Early Life Nutritional Insults to Later Programmed Hypertension and Metabolic Syndrome.International journal of molecular sciences · 2015Review
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimPeroxisome proliferator activated receptors (PPARs) are nuclear transcription factors that regulate numerous genes influencing blood pressure. The aim of this study was to examine the effects of clofibrate, a PPARα ligand, on blood pressure in spontaneously hypertensive rats (SHR).
methodsWistar-Kyoto (WKY) and spontaneously hypertensive rats (SHR), 8-9 weeks old, were randomly allocated into groups treated with vehicle or clofibrate (250 mg·kg(-1)·d(-1), ip for 21 d). Systolic blood pressure (SBP) was measured before and after the study period using tail-cuff plethysmography. Rats were sacrificed under anesthesia and blood, urine and tissue samples were processed for subsequent analysis.
resultsSHR rats showed significantly higher SBP compared with WKY rats (198±6 mmHg vs 93±7 mmHg), and a 3-fold increase in urinary protein excretion. Clofibrate treatment reduced SBP by 26%±2% and proteinuria by 43%±9% in SHR but not in WKY rats. The urinary nitrite/nitrate excretion in SHR rats was nearly 2-fold greater than that in WKY, and was further increased by 30%±4% and 48%±3%, respectively, following clofibrate treatment. In addition, PPARα protein expression and PPARα activity were significantly lower in SHR than that in WKY rats. Clofibrate treatment significantly increased PPARα protein expression and PPARα activity in SHR rats, but not in WKY rats. Moreover, the vasoconstrictor response of aortic ring was markedly increased in SHRs, which was blunted after clofibrate treatment.
conclusionPPARα contributes to regulation of blood pressure and vascular reactivity in SHR, and clofibrate-mediated reduction in blood pressure and proteinuria is probably through increased NO production.
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