PPARα stimulation exerts a blood pressure lowering effect through different mechanisms in a time-dependent manner

Ibarra-Lara, Luz; Cervantes-Pérez, Luz Graciela; Pérez-Severiano, Francisca; Valle, Leonardo del; Rubio-Ruíz, Esther; Soria-Castro, Elizabeth; Pastelín-Hernández, Gustavo; Sánchez-Aguilar, María; Martínez-Lazcano, Juan Carlos; Sánchez-Mendoza, Alicia

doi:10.1016/j.ejphar.2009.10.039

Cited by 25 publications

(27 citation statements)

References 35 publications

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“…Indeed, PPARs activation both stimulates the expression of the antioxidant enzyme superoxide dismutase and catalase, and regulates glutathione metabolism in several cell types (Lin et al 2007, Abdelmegeed et al 2009, Ibarra-Lara et al 2010. Activation of PPARa also regulates lipid peroxidation, a regulation evident in plasma and tissues in different pathologies and inflammatory conditions including the diabetic state (Inoue et al 1997, Anwer et al 2007, Belfort et al 2010.…”

Section: Discussionmentioning

confidence: 99%

“…Activation of PPARa also regulates lipid peroxidation, a regulation evident in plasma and tissues in different pathologies and inflammatory conditions including the diabetic state (Inoue et al 1997, Anwer et al 2007, Belfort et al 2010. NO production is negatively regulated by PPARa activation in different tissues, through a mechanism in part related to the reduction of iNOS concentrations (Paukkeri et al 2007, Cuzzocrea et al 2008, Ibarra-Lara et al 2010. In this study, we found that PPARa activation negatively regulates lipid peroxidation and NO production in the placenta, an effect that is particularly relevant in maternal diabetes, in which the excess of reactive oxygen and nitrogen species are clearly related to the damaging effects in placental tissues (Jawerbaum & Gonzalez 2006, Webster et al 2008).…”

Section: Discussionmentioning

confidence: 99%

“…Besides, PPARa activation prevents lipid peroxidation and regulates anti-inflammatory pathways in several tissues (Cuzzocrea et al 2008, Belfort et al 2010. In addition, when PPARa is activated, NO generation is inhibited in various tissues and cell types, in part by reducing the concentrations of the inducible form of NO synthase (iNOS; Paukkeri et al 2007, Cuzzocrea et al 2008, Ibarra-Lara et al 2010.…”

Section: Introductionmentioning

confidence: 99%

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PPARα agonists regulate lipid metabolism and nitric oxide production and prevent placental overgrowth in term placentas from diabetic rats

Martínez¹,

Kurtz²,

Capobianco³

et al. 2011

Journal of Molecular Endocrinology

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Maternal diabetes impairs fetoplacental metabolism and growth. Peroxisome proliferator-activated receptor a (PPARa) is a nuclear receptor capable of regulating lipid metabolism and inflammatory pathways. In this study, we analyzed whether placental and fetal PPARa activation regulates lipid metabolism and nitric oxide (NO) production in term placentas from diabetic rats. Diabetes was induced by neonatal streptozotocin administration. On day 21 of pregnancy, placentas from control and diabetic rats were cultured in the presence of PPARa agonists (clofibrate and leukotriene B 4 (LTB 4 )) for further evaluation of levels, synthesis, and peroxidation of lipids as well as NO production. Besides, on days 19, 20, and 21 of gestation, fetuses were injected with LTB 4 , and the placentas were explanted on day 21 of gestation for evaluation of placental weight and concentrations of placental lipids, lipoperoxides, and NO metabolites. We found that placentas from diabetic rats showed reduced PPARa concentrations. They presented no lipid overaccumulation but reduced lipid synthesis, parameters negatively regulated by PPARa activators. Lipid peroxidation and NO production, increased in placentas from diabetic rats, were negatively regulated by PPARa activators. Fetal PPARa activation in diabetic rats does not change placental lipid concentrations but reduced placental weight and NO production. In conclusion, PPARa activators regulate lipid metabolism and NO production in term placentas from diabetic rats, an activation that regulates placental growth and can partly be exerted by the developing fetus.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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PPARα agonists regulate lipid metabolism and nitric oxide production and prevent placental overgrowth in term placentas from diabetic rats

Martínez¹,

Kurtz²,

Capobianco³

et al. 2011

Journal of Molecular Endocrinology

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“…PPARα activation has been reported to stimulate endothelial nitric oxide (NO) synthesis [9] , improve endothelial-mediated NO vasodilation [10] , and increase urinary excretion of NO in the rat [11] . The beneficial effect for PPARα in cardiovascular diseases has therefore been suggested to involve the NO/NO synthase and was ascribed to the antiatherogenic and anti-inflammatory actions of NO [12] .…”

Section: Introductionmentioning

confidence: 99%

“…PPARs, as transcriptional regulators have been implicated as regulator of expression and activity of endogenous vasoconstrictors as well as their receptors. Therefore, it is possible that induction of PPARα may attenuate vasoconstriction response to major endogenous vasoconstrictor such as AII, thromboxane A2 (TXA 2 ) and endothelin 1 (ET-1) [2,12] .…”

Section: Introductionmentioning

confidence: 99%

PPARα ligand clofibrate ameliorates blood pressure and vascular reactivity in spontaneously hypertensive rats

Yousefipour

Newaz

2014

Acta Pharmacol Sin

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Aim: Peroxisome 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). Methods: Wistar-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. Results: SHR 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. Conclusion: PPARα 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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Unsalted tomato juice intake improves blood pressure and serum low‐density lipoprotein cholesterol level in local Japanese residents at risk of cardiovascular disease

Odai

Terauchi

Okamoto³

et al. 2019

Food Science & Nutrition

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The aim of this study was to investigate the effects of unsalted tomato juice intake on cardiovascular risk markers in local Japanese residents. Four hundred and eighty‐one local residents in Kuriyama, Japan, were enrolled in this study. Throughout the year of the study, they were provided with as much unsalted tomato juice as they wanted. Participants were screened for cardiovascular risk markers, such as blood pressure (BP), serum lipid profile, and glucose tolerance, before and after the study period. Of the study participants, 260 participated in a detailed study of their lifestyle factors. The average ages of the 184 male and 297 female participants were 56.3 ± 13.3 (mean ± SD ) and 58.4 ± 11.7 years, respectively. BP in 94 participants with untreated prehypertension or hypertension was significantly lowered (systolic BP, 141.2 ± 12.1–137.0 ± 16.3 mmHg, p = 0.003; diastolic BP, 83.3 ± 10.1–80.9 ± 11.1 mmHg, p = 0.012, paired t test). Further, the serum low‐density lipoprotein cholesterol (LDL‐C) level in 125 participants with untreated dyslipidemia significantly decreased (155.0 ± 23.2–149.9 ± 25.0 mg/dl, p = 0.005, paired t test). These beneficial effects were not different between sexes and among the different age groups. No significant difference in lifestyle was found before and after the study. Unsalted tomato juice intake improved systolic and diastolic BP and serum LDL‐C level in local Japanese residents at risk of cardiovascular conditions.

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PPARα stimulation exerts a blood pressure lowering effect through different mechanisms in a time-dependent manner

Cited by 25 publications

References 35 publications

PPARα agonists regulate lipid metabolism and nitric oxide production and prevent placental overgrowth in term placentas from diabetic rats

PPARα agonists regulate lipid metabolism and nitric oxide production and prevent placental overgrowth in term placentas from diabetic rats

PPARα ligand clofibrate ameliorates blood pressure and vascular reactivity in spontaneously hypertensive rats

Unsalted tomato juice intake improves blood pressure and serum low‐density lipoprotein cholesterol level in local Japanese residents at risk of cardiovascular disease

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