Resveratrol decreases calcium sensitivity of vascular smooth muscle and enhances cytosolic calcium increase in endothelium

Buluç, M.; Demirel-Yılmaz, Emine

doi:10.1016/j.vph.2005.12.003

Cited by 42 publications

(41 citation statements)

References 29 publications

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“…[30][31][32][33] The mechanism is still unknown. However, impaired endothelial activity, 30) increased response to Ca 2ϩ , 34) increase in vasoconstrictor prostanoids due to increase superoxide anion (prostaglandin F2 alpha (PGF 2a )) or prostaglandin H 2 /thromboxane A 2 ) 35) might be responsible for increased contraction responses in diabetic rats, which could be improved by RSV treatment.…”

Section: Discussionmentioning

confidence: 99%

The Effects of Chronic Resveratrol Treatment on Vascular Responsiveness of Streptozotocin-Induced Diabetic Rats

Silan

2008

Biological & Pharmaceutical Bulletin

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Resveratrol (3,4Ј,5-trihydroxystilbene) (RSV) is found in dietary plants, and it is a phytoalexin substantially present in grapes and wines, especially in red wines. Resveratrol has been reported to possess a wide range of pharmacological effects, including anti-inflammatory, anticarcinogenic, antioxidant, estrogenic, antiplatelet, and antimicrobial properties. [1][2][3][4][5][6][7] Resveratrol in red wine has been suggested to be responsible for the "French paradox", decreased risk for coronary artery disease in France.8) The beneficial effects of these compounds seem to be due to their antioxidant/antiradical activities protecting the vascular walls from oxidation, inflammation, platelet aggregation, and thrombus formation. 9)Several reports point to protective acute effects of resveratrol on vascular bed, most indicating its vasodilator effects through direct and/or endothelium dependent mechanisms. [10][11][12] The key regulators of the vasomotor function are vasodilatator nitride oxide (NO) and the vasoconstrictor endothelin-1 (ET-1). Alnaeb et al. demonstrated the number of ET-1 receptors was significantly higher whereas, the expression of endothelial NO synthase (eNOS) was significantly lower when comparing aortas from normal rabbits with these from diabetics ones.13) eNOS expression in aorta was significantly lower in insulin-resistant and diabetes mellitus (DM) rats compared with normal control rats and the decrease was more pronounced in DM rats.14) Resveratrol significantly increased the expression of the gene encoding eNOS, which synthesis the vasodilator molecule NO, and decreased expression of the potent vasoconstrictor, endothelin-1 (ET-1). 15)Resveratrol reduces the generation of H 2 O 2 and normalizes the levels of oxidized glutathione reductase and myeloperoxidase (MPO) activities. By normalization of the reductive oxygen species (ROS) levels, resveratrol limits the oxidative stress, which inhibits NO synthesis by eNOS necessary for vasorelaxation.9) Resveratrol inhibits ET-1 promoter activity, ET-1 mRNA level and strain induced ET-1 secretion. Furthermore, resveratrol inhibits ET-1 surproduction and cytosolic phospholipase A 2 activity stimulated by oxidative stress. 9)Diabetes mellitus is an important health problem and mortality from cardiovascular complications is almost three fold higher in the diabetic population than in the general population.16,17) Oxidative stress is a major factor in the genesis of both macroangiopathy and microangiopathy in diabetes. 18)Unlike single angiogenic factor antagonists, resveratrol has therapeutic value (even at very low concentrations of 1-2.5 mM), as it blocks multiple angiogenic pathways including protein kinase C, vascular endothelial growth factor and cyclooxygenase.9) Resveratrol might have a protective effect on diabetic vascular degeneration with its vasorelaxant, antiangiogenic and hypoglycemic features.The purpose of this study was to investigate the chronic effects of resveratrol on diabetes and vascular response in streptozotocin (STZ) induced ...

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Section: Discussionmentioning

confidence: 99%

The Effects of Chronic Resveratrol Treatment on Vascular Responsiveness of Streptozotocin-Induced Diabetic Rats

Silan

2008

Biological & Pharmaceutical Bulletin

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“…Differences from control (*) and DOCA salt (?). Values are expressed as mean ± SEM (n = [8][9][10][11][12][13][14][15] reported [5][6][7]. In our study, DOCA salt-induced hypertension was prevented by resveratrol but, blood pressure of the normal animals was not affected.…”

Section: Discussionmentioning

confidence: 63%

“…It has been demonstrated that resveratrol has several pharmacological effects, including anti-oxidant, anti-atherogenic, anti-inflammatory, anti-platelet, anti-fungal, antiaging and anti-cancer properties [8]. In the cardiovascular system, resveratrol is able to decrease contractions in the cardiac and vascular smooth muscle [12][13][14]. In addition, the beneficial effect of resveratrol on hypertension has been Fig.…”

Section: Discussionmentioning

confidence: 99%

“…In the normotensive animals, resveratrol changed endothelium-dependent relaxations of vessels and blood level of ADMA, TAC and H 2 S. Wide ranges of pharmacological effects have been observed by resveratrol in vitro and in vivo studies [7,[12][13][14]. It is posited that metabolizing enzymes of biomarkers might be affected by resveratrol in vivo condition.…”

Section: Discussionmentioning

confidence: 99%

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Resveratrol affects histone 3 lysine 27 methylation of vessels and blood biomarkers in DOCA salt-induced hypertension

et al. 2014

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Hypertension is a risk factor for the cardiovascular diseases. Although, several drugs are used to treat hypertension, the success of the antihypertensive therapy is limited. Resveratrol decreases blood pressure in animal models of hypertension. This study researched the mechanisms behind the effects of resveratrol on hypertension. Hypertension was induced by using the deoxycorticosterone acetate (DOCA)-induced (15 mg/kg twice per week, subcutaneously) salt-sensitive hypertension model of Wistar rats. Hypertension caused a decrease in endotheliumdependent relaxations of the isolated thoracic aorta. Resveratrol treatment (50 mg/l in drinking water) prevented DOCA salt-induced hypertension, but did not improve endothelial dysfunction. Plasma nitric oxide (NO), asymmetric dimethylarginine (ADMA), total antioxidant capacity (TAC) and hydrogen sulfide (H 2 S) levels were not changed by DOCA salt application. However, treatment of resveratrol significantly decreased ADMA and increased TAC and H 2 S levels. NO level in circulation was not significantly changed by resveratrol. DOCA salt application and resveratrol treatment also caused an alteration in the epigenetic modification of vessels. Staining pattern of histone 3 lysine 27 methylation (H3K27me3) in the aorta and renal artery sections was changed. These results show that preventive effect of resveratrol on DOCA salt-induced hypertension might due to its action on the production of some blood biomarkers and the epigenetic modification of vessels that would focus upon new aspect of hypertension prevention and treatment.

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“…34 Additionally, this component shows comparable effects to indomethacin, a widely used medication for degenerative joint diseases. 35 These observations demonstrate that resveratrol has clear anti-inflammatory effects. However, the anti-inflammatory mechanism of resveratrol is unknown, and hypotheses are insufficient.…”

Section: Discussionmentioning

confidence: 82%

Resveratrol Inhibits Inflammation Induced by Heat-Killed Listeria monocytogenes

Park

Kim

Chin

et al. 2012

Journal of Medicinal Food

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Resveratrol is a polyphenolic compound in red wine that has antioxidant and cardioprotective effects in animal models. Listeria monocytogenes is a pathogen that mainly affects immunocompromised individuals and is initially detected at the cell surface or in phagosomes by toll-like receptor 2. Many antioxidants also exert anti-inflammatory activities; therefore, we evaluated the anti-inflammatory properties of resveratrol by studying the various inflammatory responses induced by heatkilled L. monocytogenes (HKLM). Resveratrol strongly blocked HKLM-induced NADPH oxidase-1 mRNA and reactive oxygen species production by macrophages. Resveratrol also suppressed monocyte chemotactic protein-1 expression, cyclooxygenase-2 expression, prostaglandin production, inducible nitric oxide (NO) synthase expression, and NO production induced by HKLM. We investigated the signaling pathway involved in the resveratrol effect. HKLM stimulated glycogen synthase kinase 3b (GSK3b) and extracellular signal-regulated kinase 1/2 (ERK1/2) phosphorylation. The involvement of GSK3b and ERK1/2 was tested using inhibitors. While the GSK3b inhibitor LiCl potentiated the effect of HKLM, the MEK inhibitor U0126 blocked these responses. Additionally, pretreatment with resveratrol blocked phosphorylation of both kinases induced by HKLM. These results suggest that HKLM is strong inducer of inflammatory mediators, and that the inhibitory effect of resveratrol may be mediated by the GSK3b and ERK1/2 pathways.KEY WORDS: COX-2 HKLM iNOS MCP-1 NADPH oxidase 1 resveratrol

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Resveratrol decreases calcium sensitivity of vascular smooth muscle and enhances cytosolic calcium increase in endothelium

Cited by 42 publications

References 29 publications

The Effects of Chronic Resveratrol Treatment on Vascular Responsiveness of Streptozotocin-Induced Diabetic Rats

The Effects of Chronic Resveratrol Treatment on Vascular Responsiveness of Streptozotocin-Induced Diabetic Rats

Resveratrol affects histone 3 lysine 27 methylation of vessels and blood biomarkers in DOCA salt-induced hypertension

Resveratrol Inhibits Inflammation Induced by Heat-Killed Listeria monocytogenes

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