Elevated blood pressure in spontaneously hypertensive rats consuming a high sucrose diet is associated with elevated angiotensin II and is reversed by vanadium

Shi, Shang-Jin; Preuss, Harry G.; Abernethy, Darrell; Li, Xin; Jarrell, S. Taylor; Andrawis, Nabil S.

doi:10.1097/00004872-199715080-00009

Cited by 23 publications

(14 citation statements)

References 23 publications

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“…In addition to our finding of microvascular dysfunction and depressed NO signaling, sucrose-induced hypertension is related to other pathogenic factors including elevated plasma renin activity [73] and angiotensin II [74], peripheral sympathetic activation [75,76,77], and abnormal sodium and water homeostasis [78]. Whether these perturbations are influenced by dietary Cr 3 remains to be determined.…”

Section: Discussionmentioning

confidence: 87%

Effect of Dietary Chromium on Resistance Artery Function and Nitric Oxide Signaling in the Sucrose-Fed Spontaneously Hypertensive Rat

2007

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Background: Consumption of high-glycemic index foods contributes to the development of hypertension in some patients. Likewise, in spontaneously hypertensive rats (SHR), high sucrose promotes a secondary rise in systolic blood pressure (SBP). Chromium (III) (Cr³⁺) prevents sucrose-induced hypertension, but leaves the basal hypertension that characterizes SHR intact. Methods: Since hypertension entails increased peripheral resistance, we compared effects of Cr³⁺ on resistance arteries from SHR fed low-glycemic (starch) versus high-glycemic (sucrose) index diets. Subgroups of SHR also received Cr³⁺. Structure, stiffness, and vasodilation of mesenteric resistance arteries were studied using pressurized myography. Results: Sucrose increased SBP in SHR and, exclusively in sucrose-fed SHR, Cr³⁺ reduced SBP and augmented acetylcholine or nitroprusside-dependent vasodilation. Neither sucrose nor Cr³⁺ affected artery structure or stiffness. Since Cr³⁺ enhanced vasodilation, we assessed endothelial NO synthase (eNOS), guanylate cyclase, cGMP-dependent protein kinase (PKG-1α and 1β), and PKG activity by immunoblotting. Sucrose reduced eNOS, PKG-1β, and PKG activity. Cr³⁺ prevented the effects of sucrose on NO signaling. Conclusion: In hypertension exacerbated by high-glycemic index diet, Cr³⁺ reduces SBP. The BP-lowering effect of Cr³⁺, selectively on sucrose-induced but not basal hypertension in SHR, involves at least in part, improving vasodilatory function vis-à-vis restoration of NO signaling in resistance arteries.

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Section: Discussionmentioning

confidence: 87%

Effect of Dietary Chromium on Resistance Artery Function and Nitric Oxide Signaling in the Sucrose-Fed Spontaneously Hypertensive Rat

2007

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“…1). Since GSH was found to be involved in vanadate bioreduction [10][11][12][13][14][15], the levels of GSH should be affected when vanadate is administered. Indeed, it has been reported that the GSH pool is enhanced in the presence of vanadate [23,39].…”

Section: Resultsmentioning

confidence: 99%

“…Vanadium can induce the formation of reactive oxygen species (ROS) in biological systems through: (i) Fenton-like reactions [9]; (ii) vanadate bioreduction mediated by reduced glutathione (GSH), flavoenzymes or NAD(P)H oxidases with ROS as a by-product [10][11][12][13][14][15]; (iii) and recent evidences point out to an indirect promotion of ROS production, probably by interacting with mitochondria [16]. Moreover, vanadium toxicological effects in several cell types have been related with ROS production [16][17][18][19].…”

Section: Introductionmentioning

confidence: 99%

Vanadate oligomers: In vivo effects in hepatic vanadium accumulation and stress markers

Gândara

Soares

Martins

et al. 2005

Journal of Inorganic Biochemistry

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The formation of vanadate oligomeric species is often disregarded in studies on vanadate effects in biological systems, particularly in vivo, even though they may interact with high affinity with many proteins. We report the effects in fish hepatic tissue of an acute intravenous exposure (12, 24 h and 7 days) to two vanadium(V) solutions, metavanadate and decavanadate, containing different vanadate oligomers administered at sub-lethal concentration (5 mM; 1 mg/kg). Decavanadate solution promotes a 5-fold increase (0.135 ± 0.053 lg V À1 dry tissues) in the vanadium content of the mitochondrial fraction 7 days after exposition, whereas no effects were observed after metavanadate solution administration. Reduced glutathione (GSH) levels did not change and the overall reactive oxygen species (ROS) production was decreased by 30% 24 h after decavanadate administration, while for metavanadate, GSH levels increased 35%, the overall ROS production was depressed by 40% and mitochondrial superoxide anion production decreased 45%. Decavanadate intoxication did not induce changes in the rate of lipid peroxidation till 12 h, but later increased 80%, which is similar to the increase observed for metavanadate after 24 h. Decameric vanadate administration clearly induces different effects than the other vanadate oligomeric species, pointing out the importance of taking into account the different vanadate oligomers in the evaluation of vanadium(V) effects in biological systems.

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“…Several biological studies associate vanadium with the ability to produce reactive oxygen species (ROS) resulting in antioxidant enzymes alterations and leading to lipid peroxidation [1][2][3][4][5][6][7][8]. The involvement of toxic metals in cardiac oxidative damage suggests that this organ shows a great vulnerability to metal intoxication [9][10][11][12].…”

Section: Introductionmentioning

confidence: 99%

Vanadium distribution, lipid peroxidation and oxidative stress markers upon decavanadate in vivo administration

Soares

Martins

Duarte

et al. 2007

Journal of Inorganic Biochemistry

110

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The contribution of decameric vanadate species to vanadate toxic effects in cardiac muscle was studied following an intravenous administration of a decavanadate solution (1 mM total vanadium) in Sparus aurata. Although decameric vanadate is unstable in the assay medium, it decomposes with a half-life time of 16 allowing studying its effects not only in vitro but also in vivo. After 1, 6 and 12 h upon decavanadate administration the increase of vanadium in blood plasma, red blood cells and in cardiac mitochondria and cytosol is not affected in comparison to the administration of a metavanadate solution containing labile oxovanadates. Cardiac tissue lipid peroxidation increases up to 20%, 1, 6 and 12 h after metavanadate administration, whilst for decavanadate no effects were observed except 1 h after treatment (+20%). Metavanadate administration clearly differs from decavanadate by enhancing, 12 h after exposure, mitochondrial superoxide dismutase (SOD) activity (+115%) and not affecting catalase (CAT) activity whereas decavanadate increases SOD activity by 20% and decreases (À55%) mitochondrial CAT activity. At early times of exposure, 1 and 6 h, the only effect observed upon decavanadate administration was the increase by 20% of SOD activity. In conclusion, decavanadate has a different response pattern of lipid peroxidation and oxidative stress markers, in spite of the same vanadium distribution in cardiac cells observed after decavanadate and metavanadate administration. It is suggested that once formed decameric vanadate species has a different reactivity than vanadate, thus, pointing out that the differential contribution of vanadium oligomers should be taken into account to rationalize in vivo vanadate toxicity.

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Elevated blood pressure in spontaneously hypertensive rats consuming a high sucrose diet is associated with elevated angiotensin II and is reversed by vanadium

Cited by 23 publications

References 23 publications

Effect of Dietary Chromium on Resistance Artery Function and Nitric Oxide Signaling in the Sucrose-Fed Spontaneously Hypertensive Rat

Effect of Dietary Chromium on Resistance Artery Function and Nitric Oxide Signaling in the Sucrose-Fed Spontaneously Hypertensive Rat

Vanadate oligomers: In vivo effects in hepatic vanadium accumulation and stress markers

Vanadium distribution, lipid peroxidation and oxidative stress markers upon decavanadate in vivo administration

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