Effects of an L-arginine-based multi ingredient product on endothelial function in subjects with mild to moderate hypertension and hyperhomocysteinemia - a randomized, double-blind, placebo-controlled, cross-over trial

Reule, Claudia; Goyvaerts, Birgit; Schoen, Christiane

doi:10.1186/s12906-017-1603-9

Cited by 20 publications

(51 citation statements)

References 28 publications

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“…Endothelial dysfunction is the first step leading from decreased vascular dilatation up to hypertension and other cardiovascular disorders. This fact was confirmed not only in experimental (Liu et al , 2017 ) but also in clinical studies (Reule et al , 2017 ) and is in accordance with our findings.…”

Section: Discussionsupporting

confidence: 93%

Monotherapy of experimental metabolic syndrome: II. Study of cardiovascular effects

Knézl

Sotníková

Brnoliaková

et al. 2017

Interdisciplinary Toxicology

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Metabolic syndrome belongs to the most important risk factors of cardiovascular diseases. The aim of this study was to investigate changes in cardiovascular system induced by high cholesterol and high fat diet (HCHF) in HTG rats and their influence by a pyridoindole antioxidant – SMe1EC2 (S). The effects of S were compared with those of atorvastatin (A). Male HTG rats were fed HCHF (1% cholesterol + 7.5% lard) for 4 weeks. S and A were administered p.o., 50 mg/kg b.w. Following experimental groups were used: Wistar rats (W), hypertriglyceridemic rats (HTG), HTG rats fed HCHF (CHOL), HTG+S (S-HTG), CHOL+S (S-CHOL), and CHOL+A (A-CHOL). Values of blood pressure (BP) and selected ECG parameters were monitored in conscious animals, functions of the isolated heart and aorta were analyzed ex vivo. At the end of the experiment, systolic (sBP) and diastolic (dBP) blood pressure was increased in HTG and CHOL. S and A decreased BP in all treated groups. Accordingly with BP changes, the aortic endothelial function of CHOL was damaged. Both S and A administration ameliorated the endothelium-dependent relaxation to values of W. PQ and QTc intervals were prolonged in CHOL, while the treatment with S or A improved ECG findings. Prodysrhythmogenic threshold was decreased significantly in CHOL and both treatments returned it to the control values. In conclusion, HCHF increased BP, impaired endothelial relaxation of the aorta and potentiated susceptibility of myocardium to dysrhythmias. The effect of S on the changes induced by HCHF diet was more pronounced than that of A.

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Section: Discussionsupporting

confidence: 93%

Monotherapy of experimental metabolic syndrome: II. Study of cardiovascular effects

Knézl

Sotníková

Brnoliaková

et al. 2017

Interdisciplinary Toxicology

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“…HHcy promotes oxidative stress, which induces endothelial dysfunction leading to atherosclerosis and other cardiovascular diseases. Clinical in vivo studies have confirmed the occurrence of endothelial dysfunction in HHcy . To assess a potential mechanism of the effect of HHcy on cardiac function, we measured oxidative stress indicators and the activity of the antioxidant enzyme system (Figure ).…”

Section: Discussionmentioning

confidence: 99%

Vitamin B complex mitigates cardiac dysfunction in high‐methionine diet‐induced hyperhomocysteinemia

Jeremić

Turnic

Živković

et al. 2018

Clin Exp Pharma Physio

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This research is designed to test the hypothesis that elevated homocysteine (Hcy) levels in vivo, caused by a deficit in vitamin B complex, promote changes in cardiac function and redox status that lead to heart failure. In order to conduct the study, we used adult male Wistar albino rats (n = 30; 4 weeks old; 100 ± 15 g body weight). Hyperhomocysteinaemia (HHcy) in these animals was achieved by dietary manipulation. For 4 weeks, the animals were fed with a standard rodent chow (control, CF), a diet enriched in methionine with no deficiency in B vitamins (i.e., folic acid, B6 and B12) (HMNV) or a diet enriched in methionine and deficient in B vitamins (HMLV). After 28 days of dietary manipulation, all animals were killed. The rat hearts were isolated and retrogradely perfused according to the Langendorff technique at a gradually increasing perfusion pressure. We found a negative correlation between elevated serum Hcy and total body and heart weight. The maximum rate of left ventricular pressure development was significantly increased in the HMNV group compared with in the other groups. Systolic left ventricular pressure was significantly changed in all groups. HHcy induces remodelling of the cardiac tissues, as moderate HHcy is associated with more prominent interstitial and perivascular fibrosis. Our results suggest that a high methionine diet without vitamin B complex causes profound negative effects associated with HHcy.

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“…A recent meta-analysis indicates that doses between 4 and 24 g/day decrease blood pressure (systolic, 5 mmHg; diastolic, 3 mmHg) (240). Other recent studies show improved endothelial function and insulin sensitivity in patients with impaired glucose uptake and metabolic syndrome (6.6 g/day L-arginine for 2 wk) (663) and improved endothelial function and decreased homocysteine levels in patients with elevated blood pressure and hyperhomocysteinuria (2.4 g/day for 4 wk) (781).…”

Section: Pharmacological Interventions In Enos Uncouplingmentioning

confidence: 94%

Sources of Vascular Nitric Oxide and Reactive Oxygen Species and Their Regulation

Tejero

Shiva

Gladwin

2019

Physiological Reviews

400

276

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Nitric oxide (NO) is a small free radical with critical signaling roles in physiology and pathophysiology. The generation of sufficient NO levels to regulate the resistance of the blood vessels and hence the maintenance of adequate blood flow is critical to the healthy performance of the vasculature. A novel paradigm indicates that classical NO synthesis by dedicated NO synthases is supplemented by nitrite reduction pathways under hypoxia. At the same time, reactive oxygen species (ROS), which include superoxide and hydrogen peroxide, are produced in the vascular system for signaling purposes, as effectors of the immune response, or as byproducts of cellular metabolism. NO and ROS can be generated by distinct enzymes or by the same enzyme through alternate reduction and oxidation processes. The latter oxidoreductase systems include NO synthases, molybdopterin enzymes, and hemoglobins, which can form superoxide by reduction of molecular oxygen or NO by reduction of inorganic nitrite. Enzymatic uncoupling, changes in oxygen tension, and the concentration of coenzymes and reductants can modulate the NO/ROS production from these oxidoreductases and determine the redox balance in health and disease. The dysregulation of the mechanisms involved in the generation of NO and ROS is an important cause of cardiovascular disease and target for therapy. In this review we will present the biology of NO and ROS in the cardiovascular system, with special emphasis on their routes of formation and regulation, as well as the therapeutic challenges and opportunities for the management of NO and ROS in cardiovascular disease.

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Effects of an L-arginine-based multi ingredient product on endothelial function in subjects with mild to moderate hypertension and hyperhomocysteinemia - a randomized, double-blind, placebo-controlled, cross-over trial

Cited by 20 publications

References 28 publications

Monotherapy of experimental metabolic syndrome: II. Study of cardiovascular effects

Monotherapy of experimental metabolic syndrome: II. Study of cardiovascular effects

Vitamin B complex mitigates cardiac dysfunction in high‐methionine diet‐induced hyperhomocysteinemia

Sources of Vascular Nitric Oxide and Reactive Oxygen Species and Their Regulation

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