scholarly journals Potential mechanisms for the effects of far-infrared on the cardiovascular system – a review

VASA ◽  
2019 ◽  
Vol 48 (4) ◽  
pp. 303-312 ◽  
Author(s):  
Richard Shemilt ◽  
Hala Bagabir ◽  
Chim Lang ◽  
Faisel Khan
Keyword(s):  
Nitric Oxide ◽  
Cardiovascular System ◽  
Animal Studies ◽  
Cardiovascular Health ◽  
Far Infrared ◽  
Therapeutic Effects ◽  
Beneficial Effects ◽  
Wide Range ◽  
Shock Proteins ◽  
Endothelial Nitric Oxide

Abstract. Far-infrared (FIR) is a form of thermal radiation, which may have beneficial effects on cardiovascular health. Clinical studies suggest that FIR irradiation may have therapeutic effects in heart failure, myocardial ischaemia and may improve flow and survival of arteriovenous fistula. Animal studies have suggested a wide range of potential mechanisms involving endothelial nitric oxide synthase and nitric oxide bioavailability, oxidative stress, heat shock proteins and endothelial precursor cells. However, the exact cellular and molecular mechanism of FIR on the cardiovascular system remains elusive. The purpose of this review is to discuss the current literature, focusing on mechanistic studies involving the cardiovascular system, and with a view to highlighting areas for future investigation.

scholarly journals Therapeutic Potential of Polyphenols-Loaded Polymeric Nanoparticles in Cardiovascular System

Molecules ◽  
2020 ◽  
Vol 25 (15) ◽  
pp. 3322
Author(s):  
Olga Pechanova ◽  
Ezgi Dayar ◽  
Martina Cebova
Keyword(s):  
Nitric Oxide ◽  
Cardiovascular System ◽  
Therapeutic Potential ◽  
Polymeric Nanoparticles ◽  
Ros Generation ◽  
Beneficial Effects ◽  
Natural Polyphenols ◽  
Subsequent Decrease ◽  
Endogenous Antioxidant ◽  
Endothelial Nitric Oxide

Numerous studies document an increased production of reactive oxygen species (ROS) with a subsequent decrease in nitric oxide (NO) bioavailability in different cardiovascular diseases, including hypertension, atherosclerosis, and heart failure. Many natural polyphenols have been demonstrated to decrease ROS generation and/or to induce the endogenous antioxidant enzymatic defense system. Moreover, different polyphenolic compounds have the ability to increase the activity/expression of endothelial nitric oxide synthase (eNOS) with a subsequent enhancement of NO generation. However, as a result of low absorption and bioavailability of natural polyphenols, the beneficial effects of these substances are very limited. Recent progress in delivering polyphenols to the targeted tissues revealed new possibilities for the use of polymeric nanoparticles in increasing the efficiency and reducing the degradability of natural polyphenols. This review focuses on the effects of different natural polyphenolic substances, especially resveratrol, quercetin, curcumin, and cherry extracts, and their ability to bind to polymeric nanoparticles, and summarizes the effects of polyphenol-loaded nanoparticles, mainly in the cardiovascular system.

scholarly journals Cilostazol Induces eNOS and TM Expression via Activation with Sirtuin 1/Krüppel-like Factor 2 Pathway in Endothelial Cells

2021 ◽  
Vol 22 (19) ◽  
pp. 10287
Author(s):  
Chih-Hsien Wu ◽  
Yi-Lin Chiu ◽  
Chung-Yueh Hsieh ◽  
Guo-Shiang Tsung ◽  
Lian-Shan Wu ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cells ◽  
Endothelial Nitric Oxide Synthase ◽  
Umbilical Vein ◽  
Sirtuin 1 ◽  
No Production ◽  
Beneficial Effects ◽  
Umbilical Vein Endothelial Cells ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

Cilostazol was suggested to be beneficial to retard in-stent atherosclerosis and prevent stent thrombosis. However, the mechanisms responsible for the beneficial effects of cilostazol are not fully understood. In this study, we attempted to verify the mechanism of the antithrombotic effect of cilostazol. Human umbilical vein endothelial cells (HUVECs) were cultured with various concentrations of cilostazol to verify its impact on endothelial cells. KLF2, silent information regulator transcript-1 (SIRT1), endothelial nitric oxide synthase (eNOS), and endothelial thrombomodulin (TM) expression levels were examined. We found cilostazol significantly activated KLF2 expression and KLF2-related endothelial function, including eNOS activation, Nitric oxide (NO) production, and TM secretion. The activation was regulated by SIRT1, which was also stimulated by cilostazol. These findings suggest that cilostazol may be capable of an antithrombotic and vasculoprotective effect in endothelial cells.

Abstract 15999: The Divergent Effects of Exercise Training After Myocardial Infarction or Pressure Overload Depend Critically on Endothelial Nitric Oxide Synthase

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Yanti Octavia ◽  
Elza v Deel ◽  
Monique d Waard ◽  
Martine d Boer ◽  
An Moens ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Exercise Training ◽  
Endothelial Nitric Oxide Synthase ◽  
Pressure Overload ◽  
Beneficial Effects ◽  
Enhanced Chemiluminescence ◽  
Enos Uncoupling ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

AIMS: Beneficial effects of aerobic exercise training are widely recognized. However, previously we discovered that the positive effects of exercise depend on the underlying cause of cardiac failure. Here we tested the hypothesis that endothelial nitric oxide synthase (eNOS) dependent regulation of the balance between nitric oxide and superoxide (O2•-) is critically involved in determining the effects of exercise. METHODS: Mice were exposed to 8 weeks of voluntary wheel running exercise training (EX) or sedentary housing (SED) immediately following myocardial infarction (MI), pressure overload from a transverse aortic constriction (TAC), or sham (SH) surgery. Subsequently, left ventricular (LV) ejection fraction (EF) was measured by echocardiography and Picrosirius Red staining was performed to measure collagen content. Additionally, total and NOS-dependent LV O2•- were measured using lucigenin-enhanced chemiluminescence without or with NOS inhibitor, L-NAME. eNOS uncoupling was evaluated by determining eNOS monomer dimer protein ratio and peroxynitrite (ONOO-) levels were measured through luminol-enhanced chemiluminescence. RESULTS: Cardiac dysfunction and fibrosis were ameliorated by exercise in MI but not in TAC mice (Table 1). MI and TAC both increased LV O2•- levels. Strikingly, EX diminished O2•- generation in MI, but exacerbated O2•- generation in TAC (Table 1). Furthermore, the EX-induced increase in O2•- levels in TAC were largely NOS-dependent. Accordingly, MI and TAC-induced eNOS uncoupling was normalized by EX in MI but aggravated in TAC mice (Table 1). Similarly, increased ONOO- levels following MI and TAC were diminished by EX in MI, but exacerbated by EX in TAC (Table 1). CONCLUSIONS: EX reduces eNOS-mediated cardiac oxidative stress in MI. In contrast, beneficial effects of EX are lacking in cardiac pressure-overload following TAC, due to EX-induced aggravation of ONOO- formation, eNOS uncoupling and concomitant oxidative stress.

scholarly journals The Effects of Oral l-Arginine and l-Citrulline Supplementation on Blood Pressure

Nutrients ◽  
2019 ◽  
Vol 11 (7) ◽  
pp. 1679 ◽  
Author(s):  
David Khalaf ◽  
Marcus Krüger ◽  
Markus Wehland ◽  
Manfred Infanger ◽  
Daniela Grimm
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Animal Studies ◽  
Current Data ◽  
No Production ◽  
First Pass Metabolism ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide ◽  
Antihypertensive Properties ◽  
Pass Metabolism

Nitric oxide (NO) is a well-known vasodilator produced by the vascular endothelium via the enzyme endothelial nitric oxide synthase (eNOS). The inadequate production of NO has been linked to elevated blood pressure (BP) in both human and animal studies, and might be due to substrate inaccessibility. This review aimed to investigate whether oral administration of the amino acids l-arginine (Arg) and l-citrulline (Cit), which are potential substrates for eNOS, could effectively reduce BP by increasing NO production. Both Arg and Cit are effective at increasing plasma Arg. Cit is approximately twice as potent, which is most likely due to a lower first-pass metabolism. The current data suggest that oral Arg supplementation can lower BP by 5.39/2.66 mmHg, which is an effect that is comparable with diet changes and exercise implementation. The antihypertensive properties of Cit are more questionable, but are likely in the range of 4.1/2.08 to 7.54/3.77 mmHg. The exact mechanism by which Cit and Arg exert their effect is not fully understood, as normal plasma Arg concentration greatly exceeds the Michaelis constant (Km) of eNOS. Thus, elevated plasma Arg concentrations would not be expected to increase endogenous NO production significantly, but have nonetheless been observed in other studies. This phenomenon is known as the “l-arginine paradox”.

scholarly journals Statin-Induced Nitric Oxide Signaling: Mechanisms and Therapeutic Implications

2019 ◽  
Vol 8 (12) ◽  
pp. 2051 ◽  
Author(s):  
Armita Mahdavi Gorabi ◽  
Nasim Kiaie ◽  
Saeideh Hajighasemi ◽  
Maciej Banach ◽  
Peter E. Penson ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Heart Failure ◽  
Blood Pressure ◽  
Atherosclerotic Plaques ◽  
Therapeutic Effects ◽  
Therapeutic Implications ◽  
Nitric Oxide Signaling ◽  
Beneficial Effects ◽  
Signaling Mechanisms ◽  
Neurological Injuries

In addition to their cholesterol-lowering effects, statins are associated with pleiotropic effects including improvements in heart failure (HF), reduced blood pressure, prevention of the rupture of atherosclerotic plaques and improved angiogenesis. In addition to these cardiovascular benefits, statins have been implicated in the treatment of neurological injuries, cancer, sepsis, and cirrhosis. These cholesterol-independent beneficial effects of statins are predominantly mediated through signaling pathways leading to increased production and bioavailability of nitric oxide (NO). In this review, the mechanistic pathways and therapeutic effects of statin-mediated elevations of NO are described and discussed.

Pharmacokinetics of L-arginine during chronic administration to patients with hypercholesterolaemia

1999 ◽  
Vol 96 (2) ◽  
pp. 199-207 ◽  
Author(s):  
Oranee TANGPHAO ◽  
Stephan CHALON ◽  
Heitor MORENO ◽  
Brian B. HOFFMAN ◽  
Terrence F. BLASCHKE
Keyword(s):  
Nitric Oxide ◽  
Animal Studies ◽  
Peak Plasma ◽  
Plasma Concentrations ◽  
Area Under The Curve ◽  
Chronic Administration ◽  
Pharmacokinetic Studies ◽  
Acute Administration ◽  
Term Administration ◽  
Endothelial Nitric Oxide

Acute administration of L-arginine, the precursor of endothelial nitric oxide, has been shown to improve endothelial function in hypercholesterolaemic rabbits and humans. Animal studies suggest that this beneficial effect, which is thought to be related to the increased availability of nitric oxide, may not be sustained during chronic oral administration. Pharmacokinetic alterations may contribute to this observation. The present study was designed to examine the disposition of L-arginine in hypercholesterolaemic subjects during long-term administration. Plasma L-arginine concentrations were determined by HPLC in 10 patients (eight women and two men; mean age 46±16 years) after an intravenous dose of 10 or 30 g and an oral dose of 5 or 7 g. Pharmacokinetic studies were performed at regular intervals (4 weeks) during a 12-week period of oral L-arginine administration (14–21 g/day). The average plasma L-arginine concentrations before (baseline) and during administration were 16.1±1.2 and 22.5±1.3 μg/ml respectively (P< 0.05). Plasma concentrations of L-arginine remained above baseline throughout weeks 2–12. The L-arginine exposure, expressed as a normalized area-under-the-curve for 8 h (AUC0–8) after oral or intravenous doses during the first visit, was 894.4±118.7 and 1837.8±157.0 units respectively. There were no significant changes in peak plasma L-arginine concentrations or in the AUC0–8 after oral and intravenous doses during subsequent visits (P> 0.05). The mean non-renal clearance of L-arginine during the four visits remained constant. Knowledge of the pharmacokinetics of L-arginine may be useful in the design of clinical trials involving this agent, as well as in the interpretation of the pharmacodynamics of this important precursor of nitric oxide.

scholarly journals Anti-glycation activity of curcumin

2019 ◽  
Vol 73 ◽  
pp. 182-188
Author(s):  
Sabina Galiniak ◽  
Marek Biesiadecki ◽  
Bożena Czubat ◽  
Dorota Bartusik-Aebisher
Keyword(s):  
Curcuma Longa ◽  
Low Cost ◽  
Aldehyde Group ◽  
Secretory Cells ◽  
Therapeutic Effects ◽  
Active Inhibitor ◽  
Beneficial Effects ◽  
Wide Range

Curcumin, a compound belonging to the group of polyphenols with a characteristic yellow-orange color, is the most active ingredient of the long-leaved Curcuma longa L. and the ingredient of seasoning mixes, including curry spices. Due to its antioxidant, anti-inflammatory and anti-cancer properties, it has a wide range of therapeutic effects and has been studied for many years. Curcumin has enormous potential in preventing many diseases due to the widely described benefits of its use, it is non-toxic and additionally. Therapy with curcumin is low cost. Currently, many studies focus on the anti-glycation activity of curcumin, which could be used as an active inhibitor of glycation, i.e. a non-enzymatic process of combining a keto or aldehyde group of sugar with a free amino group of a protein. Finally, heterogeneous end products of advanced glycation are formed in the multistage and complicated glycation reaction. Formation of glycation products is intensified with age, as well as in various disease states, including diabetes or neurodegenerative diseases. Many literature data describe the role of curcumin in the prevention and treatment of diabetes. It is known that polyphenol has beneficial effects on hyperglycemia, insulin resistance and regeneration of secretory cells of pancreatic islets. It seems that addition of curcumin, the main ingredient of curry spice, to food could help people prevent the development of lifestyle diseases, including diabetes and its complications. The article presents the current state of knowledge on the curcumin anti-glycation properties in vitro as well as in vivo.

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