Search

Start Over Subject Nitric oxide Harvested from CDK

32. The role of PPARγ in cardiovascular diseases

Creator:
Kvandová, M., Majzúnová, M., and Dovinová, I.
Type:
article, model:article, and TEXT
Subject:
PPaRy, Hypertension, Oxidative stress, Antioxidant response, Renin-angiotensin system, and Nitric oxide
Language:
English
Description:
The peroxisome proliferator-activated receptors (PPAR) belong to the nuclear superfamily of ligand-activated transcription factors. PPARγ acts as a nutrient sensor that regulates several homeostatic functions. Its disruption can lead to vascular pathologies, disorders of fatty acid/lipid metabolism and insulin resistance. PPARγ can modulate several signaling pathways connected with blood pressure regulation. Firstly, it affects the insulin signaling pathway and endothelial dysfunction by modulation of expression and/or phosphorylation of signaling molecules through the PI3K/Akt/eNOS or MAPK/ET-1 pathways. Secondly, it can modulate gene expression of the renin- angiotensin system – cascade proteins, which potentially slow down the progression of atherosclerosis and hypertension. Thirdly, it can modulate oxidative stress response either directly through PPAR or indirectly through Nrf2 activation. In this context, activation and functioning of PPARγ is very important in the regulation of several disorders such as diabetes mellitus, hypertens ion and/or metabolic syndrome.
Rights:
http://creativecommons.org/publicdomain/mark/1.0/ and policy:public

33. The time-dependent effect of ProvinolsTM on brain NO synthase activity in L-NAME-induced hypertension

Creator:
Jendeková, L., Kojšová, S., Adriantsitohaina , R:, and Pecháňová, O.
Type:
article, model:article, and TEXT
Subject:
Red wine polyphenols, Oxidative damage, Nitric oxide, Brain, and Hypertension
Language:
English
Description:
Red wine polyphenols have been reported to possess beneficial properties for preventing cardiovascular diseases but their neuroprotective effects during chronic L-NAME treatment have not been elucidated. The aim of this study was to analyze a time course of Provinols TM effects on brain NO synthase activity and oxidative damage in L-NAME-induced hypertension. Male Wistar rats, 12 weeks old, were divided into six groups: control groups, groups treated with N G-nitro-L-arginine methyl ester (L-NAME, 40 mg/kg/day) for 4 or 7 weeks and groups receiving ProvinolsTM (40 mg/kg/day) plus L-NAME for 4 or 7 weeks. At the end of the treatment, marker of membrane oxidative damage – conjugated dienes (CD) in the brain and NO synthase activity in the cerebral cortex, cerebellum and brainstem were determined. L-NAME treatment for 4 or 7 weeks led to the increase in blood pressure, elevation of CD concentration and decrease of NO synthase activity in the brain parts investigated. ProvinolsTM partially prevented blood pressure rise and elevation of CD concentration. Comparing to the L-NAME treated group, ProvinolsTM increased NO synthase activity after 4 weeks of treatment. However, the prolonged ProvinolsTM treatment for 7 weeks had no effect on NO synthase activity decreased by L-NAME treatment. In conclusion, ProvinolsTM partially prevents L-NAME induced hypertension via the different mechanisms depending on the duration of treatment. Prevention of oxidative damage in the brain with modulating effect on NO synthase activity is suggested.
Rights:
http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public

34. Vascular effect of red wine polyphenols in chronic stress-exposed Wistar-kyoto rats

Creator:
Púzserová , A., Csizmadiová , Z. , Andriantsitohaina , R., and Bernátová, I.
Type:
article, model:article, and TEXT
Subject:
Crowding, Chronic social stress, Provinols TM, Blood pressure, and Nitric oxide
Language:
English
Description:
Present study investigated the effect of red wine polyphenolic compounds (ProvinolsTM) on blood pressure (BP), nitric oxide synthase (NOS) activity and vascular function in Wistar-Kyoto (WKY) rats exposed to chronic social stress produced by crowding. Adult male rats were divided into four groups: control (480 cm2/rat), ProvinolsTM-treated (20 mg/kg/day, 480 cm2/rat), crowded (200 cm2/rat) and crowded treated with Provinols TM (20 mg/kg/day, 200 cm2/rat) for 8 weeks. No differences in BP were observed among the groups at the end of experiment, however, reduced BP was observed in ProvinolsTM-treated rats after 3 weeks of treatment. NOS activity in the aorta was significantly elevated in crowded rats, while ProvinolsTM alone had no effect on nitric oxide (NO) production. Acetylcholine-induced relaxation of the femoral artery was significantly improved in stressed and ProvinolsTM-treated rats vs. control, without significant changes in their noradrenaline-induced vasoconstriction. Interestingly, ProvinolsTM blunted the elevation of NO production and vasorelaxation during crowding. Increased endothelium-dependent vasorelaxation and NO synthesis in crowded rats may represent the adaptation mechanisms, resulting in unaltered blood pressure in stress-exposed normotensive rats. This study further demonstrated that elevated release of NO during chronic stress may be prevented by ProvinolsTM. Thus, Provino TM might maintain equilibrium between endothelium-derived vasoconstrictor and vasodilator factors in stress.
Rights:
http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public

35. Wine Polyphenols Stimulate Superoxide Anion Production to Promote Calcium Signaling and Endothelial-Dependent Vasodilatation

Creator:
Duarte, J., Andriambeloson, E., Diebolt, M., and Adriantsitohaina, R.
Type:
article, model:article, and TEXT
Subject:
Red wine polyphenol compounds, Nitric oxide, Calcium, Superoxide anions, Endothelium, and Mesentric artery
Language:
English
Description:
The present study was aimed to evaluate the mechanisms involved in the vasorelaxant effects of red wine polyphenol compounds (RWPC) in small mesenteric rat arteries. RWPC produce relaxation in small mesenteric arteries. This relaxant effect was abolished by endothelial denudation, NO-synthase blockade with L-NAME and partial depolarization with KCl or L-NAME plus KCl. Incubation with the reactive oxygen species scavenger, superoxide dismutase (SOD) plus catalase, or inhibition of NAD(P)H-dependent oxidoreductases with diphenyleneiodonium also inhibited RWPC induced vascular relaxation. Application of RWPC elicited a transient increase in intracellular calcium concentration ([Ca2+]i) in bovine aortic endothelial cells (BAEC), which was attenuated by a mixture of SOD and catalase. Incubation of BAEC with RWPC increased the SOD inhibitable production of O2-. These results suggest the involvement of O2- in the [Ca2+]i increase evoked by RWPC, leading to the activation of enzymes involved in the release of endothelial relaxant factors and subsequent vasodilatation of resistance arteries.
Rights:
http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public