scholarly journals Soybean or Fish Oil Increases Adiponectin and Nitric Oxide Levels and Decreases Blood Pressure in Metabolic Syndrome

2012 ◽  
Vol 26 (S1) ◽  
Author(s):  
Isaias Dichi ◽  
Andréa Name Colado Simão ◽  
Marcell AB Lovozoy ◽  
Helena Kaminami Morimoto ◽  
Tathiana Name Colado Simão ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Metabolic Syndrome ◽  
Fish Oil

scholarly journals Nitric oxide enhancement and blood pressure decrease in patients with metabolic syndrome using soy protein or fish oil

2010 ◽  
Vol 54 (6) ◽  
pp. 540-545 ◽  
Author(s):  
Andréa Name Colado Simão ◽  
Marcell Alysson Batisti Lozovoy ◽  
Tathiana Name Colado Simão ◽  
Jane Bandeira Dichi ◽  
Tiemi Matsuo ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Metabolic Syndrome ◽  
Fatty Acids ◽  
Fish Oil ◽  
Soy Protein ◽  
Diastolic Pressure ◽  
Blood Pressure Reduction ◽  
Systolic Pressure ◽  
Randomized Design

OBJECTIVE: To verify the effects of fish oil and soy on nitric oxide (NO) and blood pressure in patients with metabolic syndrome (MS). SUBJECTS AND METHODS: Sixty women with MS were investigated in a parallel randomized design study. The first group maintained their usual diet; the second group received 25 g/day of soy; the third group received 3 g/day of n-3 fatty acids, and the fourth group the same amount previously cited of n-3 fatty acids and soy. RESULTS: Serum nitric oxide metabolites showed significant increase after 90 days in the fish oil and soy groups. Systolic pressure reduced after 45 days of treatment with fish oil, whereas diastolic pressure decreased significantly throughout the study in the soy group. CONCLUSIONS: NO increase and blood pressure reduction with fish oil or soy protein reinforce the importance of the influence of NO on blood pressure in patients with MS.

scholarly journals Blood pressure decrease with ingestion of a soya product (kinako) or fish oil in women with the metabolic syndrome: role of adiponectin and nitric oxide

2012 ◽  
Vol 108 (8) ◽  
pp. 1435-1442 ◽  
Author(s):  
Andréa Name Colado Simão ◽  
Marcell Alysson Batisti Lozovoy ◽  
Larissa Danielle Bahls ◽  
Helena Kaminami Morimoto ◽  
Tathiana Name Colado Simão ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Metabolic Syndrome ◽  
Fish Oil ◽  
Inflammatory Markers ◽  
Inflammatory Marker ◽  
Control Group ◽  
Treatment Groups ◽  
The Metabolic Syndrome ◽  
Baseline Values

The aim of the present study was to verify the effects of fish oil and a soya-based product on inflammatory markers and endothelial function measured by NO in women with the metabolic syndrome (MetS). A total of sixty-five women (mean age: 47·9 (sd9·98) years) were studied in a 90-d parallel, randomised design. A control group maintained their usual diet; the second group received 29 g/d of soyabean (kinako); the third group received 3 g/d of fish oiln-3 fatty acids; and the fourth group received fish oil (3 g/d) and kinako (29 g/d). Anthropometric, blood pressure (BP), inflammatory markers, anti-inflammatory marker (adiponectin) and NO concentrations were evaluated. In relation to the baseline values, the group that received fish oil and kinako concomitantly presented a statistically significant decrease in systolic BP (SBP;P < 0·05), whereas there was a significant decrease in diastolic BP (DBP) in the control group (P < 0·05), kinako group (P < 0·01) and fish oil group (P < 0·01) after 90 d. There was a significant increase in adiponectin (P < 0·01) and NO values (P < 0·05) after 90 d in the kinako and fish oil groups. Differences between treatment groups verified a significant decrease (P < 0·05) in DBP in the kinako group after 90 d when compared to the results obtained from the fish oil and kinako groups. In conclusion, the findings of increased serum adiponectin and NO metabolite levels after 90 d, both in the fish oil and soya groups, reinforce the importance of the influence of adiponectin and NO levels on BP decrease in patients with the MetS.

EGCG, a green tea polyphenol, improves endothelial function and insulin sensitivity, reduces blood pressure, and protects against myocardial I/R injury in SHR

2007 ◽  
Vol 292 (5) ◽  
pp. E1378-E1387 ◽  
Author(s):  
Maria A. Potenza ◽  
Flora L. Marasciulo ◽  
Mariela Tarquinio ◽  
Edy Tiravanti ◽  
Giuseppe Colantuono ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Metabolic Syndrome ◽  
Insulin Sensitivity ◽  
Green Tea ◽  
Ischemia Reperfusion ◽  
Egcg Treatment ◽  
Beneficial Effects ◽  
The Metabolic Syndrome ◽  
Green Tea Polyphenol

Epigallocatechin gallate (EGCG), a bioactive polyphenol in green tea, may augment metabolic and vascular actions of insulin. Therefore, we investigated effects of EGCG treatment to simultaneously improve cardiovascular and metabolic function in spontaneously hypertensive rats (SHR; model of metabolic syndrome with hypertension, insulin resistance, and overweight). In acute studies, EGCG (1–100 μM) elicited dose-dependent vasodilation in mesenteric vascular beds (MVB) isolated from SHR ex vivo that was inhibitable by Nω-nitro-l-arginine methyl ester (l-NAME; nitric oxide synthase antagonist) or wortmannin [phosphatidylinositol (PI) 3-kinase inhibitor]. In chronic studies, 9-wk-old SHR were treated by gavage for 3 wk with EGCG (200 mg·kg−1·day−1), enalapril (30 mg·kg−1·day−1), or vehicle. A separate group of SHR receiving l-NAME (80 mg/l in drinking water) was treated for 3 wk with either EGCG or vehicle. Vasodilator actions of insulin were significantly improved in MVB from EGCG- or enalapril-treated SHR (when compared with vehicle-treated SHR). Both EGCG and enalapril therapy significantly lowered systolic blood pressure (SBP) in SHR. EGCG therapy of SHR significantly reduced infarct size and improved cardiac function in Langendorff-perfused hearts exposed to ischemia-reperfusion (I/R) injury. In SHR given l-NAME, beneficial effects of EGCG on SBP and I/R were not observed. Both enalapril and EGCG treatment of SHR improved insulin sensitivity and raised plasma adiponectin levels. We conclude that acute actions of EGCG to stimulate production of nitric oxide from endothelium using PI 3-kinase-dependent pathways may explain, in part, beneficial effects of EGCG therapy to simultaneously improve metabolic and cardiovascular pathophysiology in SHR. These findings may be relevant to understanding potential benefits of green tea consumption in patients with the metabolic syndrome.

scholarly journals Effect of Melatonin on Blood Pressure and Nitric Oxide Generation in Rats With Metabolic Syndrome

2016 ◽  
pp. S373-S380 ◽  
Author(s):  
J. KLIMENTOVA ◽  
M. CEBOVA ◽  
A. BARTA ◽  
Z. MATUSKOVA ◽  
S. VRANKOVA ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Metabolic Syndrome ◽  
Protein Expression ◽  
Brain Cortex ◽  
Brain Regions ◽  
Melatonin Treatment ◽  
Protein Expressions ◽  
Oxide Synthase ◽  
The Brain

Melatonin, a multitasking indolamine, seems to be involved in a variety of physiological and metabolic processes via both receptor-mediated and receptor-independent mechanisms. The aim of our study was to find out whether melatonin can affect blood pressure (BP), nitric oxide synthase (NOS) activity, eNOS and nNOS protein expressions in rats with metabolic syndrome (SHR/cp). Rats were divided into four groups: 6-week-old male WKY andSHR/cp and age-matched WKY and SHR/cp treated with melatonin (10 mg/kg/day) for 3 weeks. BP was measured by tail-cuff plethysmography. NOS activity, eNOS and nNOS protein expressions were determined in the heart, aorta, brain cortex and cerebellum. MT1 receptors were analyzed in the brain cortex and cerebellum. In SHR/cp rats, BP was decreased after melatonin treatment. In the same group, melatonin did not affect NOS activity and eNOS protein expression in the heart and aorta, while it increased both parameters in the brain cortex and cerebellum. Interestingly, melatonin elevated MT1 protein expression in the cerebellum. Neuronal NOS protein expression was not changed within the groups. In conclusion, increased NOS activity/eNOS upregulation in particular brain regions may contribute partially to BP decrease in SHR/cp rats after melatonin treatment. Participation of MT1 receptors in this melatonin action may be supposed.

Effects of Neuroactive Amino Acids Derivatives on Cardiac and Cerebral Mitochondria and Endothelial functions in Animals Exposed to Stress

2017 ◽  
Vol 2 (2) ◽  
pp. 34
Author(s):  
TA Popova ◽  
II Prokofiev ◽  
IS Mokrousov ◽  
Valentina Perfilova ◽  
AV Borisov ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Platelet Aggregation ◽  
Atp Synthesis ◽  
Elevated Concentration ◽  
Blood Pressure Monitor ◽  
Pressure Monitor ◽  
Griess Reagent ◽  
Arterial Blood ◽  
Endothelial Functions

Introduction: To study the effects of glufimet, a new derivative of glutamic acid, and phenibut, a derivative of γ-aminobutyric acid (GABA), on cardiac and cerebral mitochondria and endothelial functions in animals following exposure to stress and inducible nitric oxide synthase (iNOS) inhibition. Methods: Rats suspended by their dorsal cervical skin fold for 24 hours served as the immobilization and pain stress model. Arterial blood pressure was determined using a non-invasive blood pressure monitor. Mitochondrial fraction of heart and brain homogenates were isolated by differential centrifugation and analysed for mitochondrial respiration intensity, lipid peroxidation (LPO) and antioxidant enzyme activity using polarographic method. The concentrations of nitric oxide (NO) terminal metabolites were measured using Griess reagent. Hemostasis indices were evaluated. Platelet aggregation was estimated using modified version of the Born method described by Gabbasov et al., 1989. Results: The present study demonstrated that stress leads to an elevated concentration of NO terminal metabolites and LPO products, decreased activity of antioxidant enzymes, reduced mitochondrial respiratory function, and endothelial dysfunction. Inhibition of iNOS by aminoguanidine had a protective effect. Phenibut and glufimet inhibited a rise in stress-induced nitric oxide production. This resulted in enhanced coupling of substrate peroxidation and ATP synthesis. The reduced LPO processes caused by glufimet and phenibut normalized the endothelial function which was proved by the absence of average daily blood pressure (BP) elevation episodes and a significant increase in platelet aggregation level. Conclusion: Glufimet and phenibut restrict the harmful effects of stress on the heart and brain possibly by modulating iNOS activity.

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