Combination Therapy with Paricalcitol and Enalapril Ameliorates Cardiac Oxidative Injury in Uremic Rats

Husain, Kazim; Ferder, León; Mizobuchi, Masahide; Finch, Jane; Slatopolsky, Eduardo

doi:10.1159/000178251

Cited by 76 publications

(75 citation statements)

References 84 publications

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“…Apart from this, the noradrenergic chronotropic response of rat atria was significantly reduced by a vitamin D depleted diet [68]. Some animal studies have already evaluated the effect of active vitamin D treatment on myocardial structure and function [69][70][71][72]. In uremic rats, treatment with the active vitamin D analog paricalcitol protected against cardiac oxidative injury [70].…”

Section: Vitamin D-deficient Ratsmentioning

confidence: 99%

“…Some animal studies have already evaluated the effect of active vitamin D treatment on myocardial structure and function [69][70][71][72]. In uremic rats, treatment with the active vitamin D analog paricalcitol protected against cardiac oxidative injury [70]. In detail, paricalcitol inhibited the superoxide-generating enzyme NADPH oxidase in the heart and increased antioxidative glutathione as well as cardiac copper/zinc superoxide dismutase activity [70].…”

Section: Vitamin D-deficient Ratsmentioning

confidence: 99%

“…In uremic rats, treatment with the active vitamin D analog paricalcitol protected against cardiac oxidative injury [70]. In detail, paricalcitol inhibited the superoxide-generating enzyme NADPH oxidase in the heart and increased antioxidative glutathione as well as cardiac copper/zinc superoxide dismutase activity [70]. In addition, Bodyak et al showed that paricalcitol treatment reduced abnormalities in left ventricular structure and function in Dahl salt-sensitive rats [71].…”

Section: Vitamin D-deficient Ratsmentioning

confidence: 99%

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Vitamin D deficiency and myocardial diseases

Pilz

Tomaschitz

Drechsler

et al. 2010

Molecular Nutrition Food Res

122

141

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Vitamin D deficiency is common among patients with myocardial diseases because sun-induced vitamin D production in the skin and dietary intake of vitamin D is often insufficient. Knockout mice for the vitamin D receptor develop myocardial hypertrophy and dysfunction. It has also been shown that children with rickets who suffered from severe heart failure could be successfully treated with supplementation of vitamin D plus calcium. In adults, almost all patients with heart failure exhibit reduced 25-hydroxyvitamin D levels, which are used to classify the vitamin D status. In prospective studies, vitamin D deficiency was an independent risk factor for mortality, deaths due to heart failure and sudden cardiac death. Several vitamin D effects on the electrophysiology, contractility, and structure of the heart suggest that vitamin D deficiency might be a causal factor for myocardial diseases. Data from interventional trials, however, are rare and urgently needed to elucidate whether vitamin D supplementation is useful for the treatment of myocardial diseases. In our opinion, the current knowledge of the beneficial effects of vitamin D on myocardial and overall health strongly argue for vitamin D supplementation in all vitamin D-deficient patients with or at high risk for myocardial diseases.

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Section: Vitamin D-deficient Ratsmentioning

confidence: 99%

Section: Vitamin D-deficient Ratsmentioning

confidence: 99%

Section: Vitamin D-deficient Ratsmentioning

confidence: 99%

See 1 more Smart Citation

Vitamin D deficiency and myocardial diseases

Pilz

Tomaschitz

Drechsler

et al. 2010

Molecular Nutrition Food Res

122

141

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“…Studies in experimental nephropathy models have focused on the effects of vitamin D and paricalcitol on glomerular damage and tubular toxicity [6][7][8]. Recently it has been shown that paricalcitol has antioxidant effects on the myocardium [9] and supresses the renin-angiotensin system (RAS) in the kidney [10].…”

mentioning

confidence: 99%

Antioxidant and renoprotective effects of paricalcitol on experimental contrast-induced nephropathy model

Arı¹,

Kedrah²,

Alahdab³

et al. 2012

The British Journal of Radiology

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Objectives: The aim of the study was to assess the effect of paricalcitol on the experimental contrast-induced nephropathy (CIN) model. We hypothesised that paricalcitol may prevent CIN. Methods: 32 Wistar albino rats were divided into four groups (n58 each): control group, paricalcitol group, CIN group and paricalcitol plus CIN group. Paricalcitol (0.4 mg kg -1 day -1 ) was given intraperitoneally for 5 consecutive days prior to induction of CIN. CIN was induced at day 4 by intravenous injection of indometacin (10 mg kg -1 ), Nv-nitro-L-arginine methyl ester (L-NAME, 10 mg kg -1 ) and meglumine amidotrizoate (6 ml kg -1 ). Renal function parameters, oxidative stress biomarkers, histopathological findings and vascular endothelial growth factor (VEGF) immunoexpression were evaluated. Results: The paricalcitol plus CIN group had lower mean serum creatinine levels (p50.034) as well as higher creatinine clearance (p50.042) than the CIN group. Serum malondialdehyde and kidney thiobarbituric acid-reacting substances levels were significantly lower in the paricalcitol plus CIN group than in the CIN group (p50.024 and p50.042, respectively). The mean scores of tubular necrosis (p50.024), proteinaceous casts (p50.038), medullary congestion (p50.035) and VEGF immunoexpression (p50.018) in the paricalcitol plus CIN group were also significantly lower. Conclusion: This study demonstrates the protective effect of paricalcitol in the prevention of CIN in an experimental model.

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“…53 Cardiac ventricular MDA levels are reportedly increased in 5/6Nx rats. 54 Circulating levels of MDA have been reported to be elevated in patients with AF, and higher baseline values of MDA can be used to predict AF recurrence after cardioversion. 55 DHLHZn, used in our study, has been shown to attenuate hepatic ischemia-reperfusion injury in rats in association with a reduction in MDA levels in the liver.…”

Section: Chronic Kidney Disease (Ckd) and Novel Antioxidant Agentmentioning

confidence: 99%