Vanadate Improves Cardiac Function and Myocardial Energy Metabolism in Diabetic Rat Hearts

Noda, Chiharu; Masuda, Takashi; Sato, Kiyotaka; Ikeda, Kazuko; Shimohama, Takao; Matsuyama, Nobuki; Izumi, Tohru

doi:10.1536/jhj.44.745

Cited by 13 publications

(7 citation statements)

References 29 publications

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“…Differences in the availability of vanadate species, concentration of vanadate, animal species, and type of the preparations, as well as experimental conditions, may be the reason for these discrepancies. Nonetheless, the present study seems to support the view that vanadate may exert beneficial effects in I/R hearts in a manner similar to that seen in hearts subjected to myocardial infarction (30) or diabetes (20).…”

Section: Discussionsupporting

confidence: 85%

“…Nonetheless, the participation of other mechanisms, such as activation of Akt, prevention of fodrin breakdown, and inhibition of apoptosis by prevention of caspase-3 activation during I/R (30), cannot be ruled out on the basis of the present study. Furthermore, the protective effect of vanadate in I/R may be associated with preservation of myocardial energy metabolism in terms of increase in myocardial contents of ATP, creatine phosphate, and cytosolic phosphorylation, as observed in diabetic hearts (20).…”

Section: Discussionmentioning

confidence: 97%

“…Alterations in cardiac function and SR Ca 2ϩ transport due to an oxyradical-generating system (xanthine ϩ xanthine oxidase) or an oxidant (H2O2) were attenuated by treatment with vanadate. These results suggest that vanadate may exert beneficial effects on cardiac performance and SR function in I/R hearts because of its antioxidant action.ischemia-reperfusion; oxidative stress VANADATE HAS BEEN OBSERVED to produce beneficial effects on cardiac function in chronic diabetes (12,20,22). This action of vanadate on diabetic heart has been mainly attributed to its insulinomimetic property of promoting glucose uptake and oxidation in the cell (10, 27, 33) as a consequence of tyrosine kinase stimulation and/or inhibition of phosphotyrosine phosphatase activities (5, 34).…”

mentioning

confidence: 92%

“…ischemia-reperfusion; oxidative stress VANADATE HAS BEEN OBSERVED to produce beneficial effects on cardiac function in chronic diabetes (12,20,22). This action of vanadate on diabetic heart has been mainly attributed to its insulinomimetic property of promoting glucose uptake and oxidation in the cell (10, 27, 33) as a consequence of tyrosine kinase stimulation and/or inhibition of phosphotyrosine phosphatase activities (5, 34).…”

mentioning

confidence: 99%

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Modification of alterations in cardiac function and sarcoplasmic reticulum by vanadate in ischemic-reperfused rat hearts

Takeda

Mochizuki²,

Saini³

et al. 2005

Journal of Applied Physiology

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. Modification of alterations in cardiac function and sarcoplasmic reticulum by vanadate in ischemicreperfused rat hearts. J Appl Physiol 99: 999 -1005, 2005. First published May 5, 2005; doi:10.1152/japplphysiol.00234.2005.-To study the cardioprotective effects of vanadate on ischemia-reperfusion (I/R) injury, isolated rat hearts perfused at constant flow were subjected to global ischemia for 30 min followed by reperfusion for 30 min. In this experimental model, I/R markedly decreased ventricular developed pressure and increased end-diastolic pressure. Pretreatment of hearts with 4 M vanadate attenuated I/R-induced cardiac dysfunction. The reduction in sarcoplasmic reticulum (SR) Ca 2ϩ uptake and Ca 2ϩ release, as well as SR protein contents for Ca 2ϩ -pump ATPase and Ca 2ϩ -release channel, was also prevented by vanadate. Pretreatment of hearts with an antioxidant mixture containing superoxide dismutase ϩ catalase exerted effects similar to those of vanadate in I/R hearts. Postischemic treatment of hearts with vanadate or superoxide dismutase ϩ catalase also had beneficial effects on I/R-induced changes in cardiac performance and SR function. Alterations in cardiac function and SR Ca 2ϩ transport due to an oxyradical-generating system (xanthine ϩ xanthine oxidase) or an oxidant (H2O2) were attenuated by treatment with vanadate. These results suggest that vanadate may exert beneficial effects on cardiac performance and SR function in I/R hearts because of its antioxidant action.ischemia-reperfusion; oxidative stress VANADATE HAS BEEN OBSERVED to produce beneficial effects on cardiac function in chronic diabetes (12,20,22). This action of vanadate on diabetic heart has been mainly attributed to its insulinomimetic property of promoting glucose uptake and oxidation in the cell (10, 27, 33) as a consequence of tyrosine kinase stimulation and/or inhibition of phosphotyrosine phosphatase activities (5, 34). Because diabetic cardiomyopathy has also been associated with oxidative stress (7), it is likely that attenuation of cardiac dysfunction in diabetes by vanadate may also be related to its antioxidant activity (17, 25). Although vanadate has been shown to scavenge oxyradicals generated by the xanthine plus xanthine oxidase (X ϩ XO) system (17), the antioxidant effect of vanadate remains to be clearly demonstrated. However, in a rat model of myocardial infarction, in which oxidative stress plays a critical role (19), the cytoprotective effect of vanadate has been shown to be associated with improvement in cardiac function, activation of phosphatidylinositol 3-kinase/protein kinase B (Akt), and inhibition of apoptosis by prevention of caspase-3 activation (30).Recently, vanadate at low concentrations (1-4 M) was found to attenuate cardiac dysfunction and changes in sarcoplasmic reticulum (SR) Ca 2ϩ uptake and ryanodine receptor (RyR)-binding activities due to ischemia-reperfusion (I/R) in isolated rat hearts (29). However, the results showing the beneficial actions of vanadate in this study (29) were not conclusive,...

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Section: Discussionsupporting

confidence: 85%

Section: Discussionmentioning

confidence: 97%

mentioning

confidence: 92%

mentioning

confidence: 99%

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Modification of alterations in cardiac function and sarcoplasmic reticulum by vanadate in ischemic-reperfused rat hearts

Takeda

Mochizuki²,

Saini³

et al. 2005

Journal of Applied Physiology

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“…Further studies demonstrate that vanadate augmented glucose uptake and improved ischemic tolerance in hypertrophied heart (84). Improvement in cardiac function following vanadate treatment may result from restoration of aberrant myocardial ATP and phophocreatine production as well as creatine kinase activities in diabetic rats (45,85,86).…”

Section: Effect Of Vanadium Compounds On the Diabetic Heartmentioning

confidence: 99%

Cardioprotection by Vanadium Compounds Targeting Akt-Mediated Signaling

Bhuiyan

Fukunaga

2009

J Pharmacol Sci

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Abstract. Treatment with inorganic and organic compounds of vanadium has been shown to exert a wide range of cardioprotective effects in myocardial ischemia/reperfusion-induced injury, myocardial hypertrophy, hypertension, and vascular diseases. Furthermore, administration of vanadium compounds improves cardiac performance and smooth muscle cell contractility and modulates blood pressure in various models of hypertension. Like other vanadium compounds, we documented bis(1-oxy-2-pyridinethiolato) oxovanadium (IV) [VO(OPT)] as a potent cardioprotective agent to elicit cardiac functional recovery in myocardial infarction and pressure overload-induced hypertrophy. Vanadium compounds activate Akt signaling through inhibition of protein tyrosine phosphatases, thereby eliciting cardioprotection in myocardial ischemia / reperfusion-induced injury and myocardial hypertrophy. Vanadium compounds also promote cardiac functional recovery by stimulation of glucose transport in diabetic heart. We here discuss the current understanding of mechanisms underlying vanadium compound-induced cardioprotection and propose a novel therapeutic strategy targeting for Akt signaling to rescue cardiomyocytes from heart failure.

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Selected Haematological and Biochemical Parameters of Blood in Rats After Subchronic Administration of Vanadium and/or Magnesium in Drinking Water

Ścibior

Zaporowska

Ostrowski

2006

Arch Environ Contam Toxicol

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The purpose of these studies was to evaluate the effect of selected vanadium and magnesium doses on certain haematological and biochemical blood parameters in rats. Outbred 2-month-old, albino male Wistar rats received for a period of 6 weeks, as a sole drinking liquid, the following water solutions: group II, sodium metavanadate (SMV) at a concentration of 0.125 mg V/mL; group III, magnesium sulphate (MS) at a concentration of 0.06 mg Mg/mL; and group IV, SMV-MS solution at the same concentrations. The control group received at this time deionized water to drink. It was calculated that group II ingested with drinking water about 10.7 mg V/kg b. w./24 h, group III 6 mg Mg/kg b. w./24 h, and group IV about 9 mg V and 4.5 mg Mg/kg b. w./24 h. The exposure to vanadium alone (group II) led to a statistically significant decrease in body weight gain, food and fluid intakes. Moreover, in the same group of rats a statistically significant decrease in the RBC count, Hb concentration, MCV, and MCH values was demonstrated. Additionally, a statistically significant decrease in the plasma L-ascorbic acid concentration and a significant increase in MDA concentration in blood in this group were found. Instead, after the administration of magnesium alone (group III), a statistically significant decrease in the fluid intake and in the L-ascorbic acid concentration in plasma was noted. Furthermore, in the same group of rats a statistically significant increase in Hb level and in the plasma magnesium concentration was demonstrated. Two-way analysis of variance (ANOVA) did not reveal the interactions between V and Mg.

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Vanadate Improves Cardiac Function and Myocardial Energy Metabolism in Diabetic Rat Hearts

Cited by 13 publications

References 29 publications

Modification of alterations in cardiac function and sarcoplasmic reticulum by vanadate in ischemic-reperfused rat hearts

Modification of alterations in cardiac function and sarcoplasmic reticulum by vanadate in ischemic-reperfused rat hearts

Cardioprotection by Vanadium Compounds Targeting Akt-Mediated Signaling

Selected Haematological and Biochemical Parameters of Blood in Rats After Subchronic Administration of Vanadium and/or Magnesium in Drinking Water

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