The angiotensin type 1 receptor antagonist valsartan attenuates pathological ventricular hypertrophy induced by hyperhomocysteinemia in rats

Kassab, Salah; Garadah, Taysir S.; Abu-Hijleh, Marwan F.; Golbahar, Jamal; Senok, Solomon S.; Wazir, Javed F.; Gumaa, K.A.

doi:10.3317/jraas.2006.039

Cited by 24 publications

(20 citation statements)

References 22 publications

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“…7 Moreover, studies using hypertensive rats showed that Hhe provoked coronary arteriolar remodeling, left ventricular hypertrophy, interstitial fibrosis, and diastolic dysfunction. 8,9 These findings were confirmed by a clinical investigation performed with Framingham Heart Study participants who proved women have a direct correlation between plasmatic Hcy concentration and left ventricular mass and wall thickness. 10 Hhe deleterious effects in cardiovascular system could be associated with different concentrations of Hcy metabolites and alterations in the metabolic pathways.…”

Section: Introductionsupporting

confidence: 74%

Homocysteine Thiolactone Induces Cardiac Dysfunction: Role of Oxidative Stress

Mendes¹,

Sirvente²,

Candido³

et al. 2010

Journal of Cardiovascular Pharmacology

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This study investigates the cardiac functioning in male Wistar rats after treatments with methionine and homocysteine thiolactone (HcyT). The rats were distributed into 3 groups and treated for 8 weeks. Group I was the control (CO) group, given water, group II was treated with methionine, and group III with HcyT (100 mg/kg). Morphometric and functional cardiac parameters were evaluated by echocardiography. Superoxide dismutase (SOD), catalase, and glutathione S-transferase activities, chemiluminescence, thiobarbituric acid reactive substances, and immunocontent were measured in the myocardium. Hyperhomocysteinemiawas observed in rats submitted to the both treatments. The results showed diastolic function was compromised in HcyT group, seen by the increase of E/A (peak velocity of early (E) and late (A) diastolic filling) ratio, decrease in deceleration time of E wave and left ventricular isovolumic relaxation time. Myocardial performance index was increased in HcyT group and was found associated with increased SOD immunocontent. HcyT group demonstrated an increase in SOD, catalase, and glutatione S-transferase activity, and chemiluminescence and thiobarbituric acid reactive substances. Overall, these results indicated that HcyT induces a cardiac dysfunction and could be associated with oxidative stress increase in the myocardium.

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Section: Introductionsupporting

confidence: 74%

Homocysteine Thiolactone Induces Cardiac Dysfunction: Role of Oxidative Stress

Mendes¹,

Sirvente²,

Candido³

et al. 2010

Journal of Cardiovascular Pharmacology

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“…By decreasing intracellular levels of ADMA, DDAH1 may prevent angiotensin II-mediated smooth muscle hypertrophy,41 perhaps leading to improved smooth muscle vasodilatory function. This potential mechanism is supported by the observation that the angiotensin II type 1 receptor antagonist valsartan protects from hyperhomocysteinemia-induced ventricular hypertrophy and vascular remodeling 42, 43…”

Section: Discussionmentioning

confidence: 94%

Overexpression of Dimethylarginine Dimethylaminohydrolase Protects Against Cerebral Vascular Effects of Hyperhomocysteinemia

Rodionov

Dayoub

Lynch

et al. 2010

Circulation Research

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Rationale: Hyperhomocysteinemia is a cardiovascular risk factor that is associated with elevation of the nitric oxide synthase inhibitor asymmetrical dimethylarginine (ADMA). Objective: Using mice transgenic for overexpression of the ADMA-hydrolyzing enzyme dimethylarginine dimethylaminohydrolase-1 (DDAH1), we tested the hypothesis that overexpression of DDAH1 protects from adverse structural and functional changes in cerebral arterioles in hyperhomocysteinemia. Methods and Results

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“…This dose is similar to that used in previous studies with this drug in rats [19,20]. Control and normal groups received distilled drinking water only.…”

Section: Valsartan Treatmentmentioning

confidence: 88%

An angiotensin II receptor antagonist reduces inflammatory parameters in two models of colitis

Santiago

Rivera

Ferder

et al. 2008

Regulatory Peptides

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Little is known about the effects of the proinflammatory hormone Angiotensin II (Ang II) in inflammatory bowel disease. The aim of this study was to evaluate the effect of Valsartan (Diovan), an Ang II receptor antagonist, in two models of colitis.METHODS-Colitis was induced in Sprague-Dawley rats by administration of trinitrobenzene sulfonic acid (TNBS; 30mg in 50% ETOH ic) or 5% Dextran Sulphate Sodium (DSS) in drinking water ad libitum for 5 days. Valsartan was administered orally in drinking water (160mg/L) during thirty days prior to the induction of the colitis, and for 5 days after. All animals were evaluated for weight change, diarrhea, myeloperoxidase activity, macroscopic and microscopic damage. Cytokine levels in the colon were measured by ELISA, real time RT-PCR and immunohistochemistry.RESULTS-In the TNBS model, Valsartan reduced the macroscopic damage score, significantly decreased the microscopic damage (p<0.01), and accelerated weight gain after colitis. In the DSS colitis model, Valsartan treated animals had less diarrhea and microscopic damage. Valsartan reduced the protein levels of TGFβ (p<0.05), and IL-18 in the TNBS model, and led to over-expression of IL-10 mRNA in the DSS model.CONCLUSION-These data demonstrate a possible anti-inflammatory effect for Valsartan in colitis.

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The angiotensin type 1 receptor antagonist valsartan attenuates pathological ventricular hypertrophy induced by hyperhomocysteinemia in rats

Abstract: Results from this study suggest that hyperhomocysteinemia-induced hypertension and ventricular hypertrophy in rats are mediated, at least partly; by Ang II activation of AT1-receptors.

Cited by 24 publications

References 22 publications

Homocysteine Thiolactone Induces Cardiac Dysfunction: Role of Oxidative Stress

Homocysteine Thiolactone Induces Cardiac Dysfunction: Role of Oxidative Stress

Overexpression of Dimethylarginine Dimethylaminohydrolase Protects Against Cerebral Vascular Effects of Hyperhomocysteinemia

An angiotensin II receptor antagonist reduces inflammatory parameters in two models of colitis

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