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ΓΚΕΛΑΝΤΟ

Το "Γκελάντο" διαφέρει από το συνηθισμένο κόκκινο κρασί, διότι για να παρασκευαστεί ένα λίτρο του χρειάζονται 5 κιλά Αγιωργήτικου σταφυλιού.

Δρ. ΔΗΜΗΤΡΙΟΣ ΝΙΚΟΛΑΟΥ ΓΚΕΛΗΣ

Ωτορινολαρυγγολόγος
Δαμασκηνού 46, Κόρινθος - 20100
Τηλ. 27410 26631, 6944280764

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Email: pharmage@otenet.gr


Polyphenols and the regulation of hypertension©

Polyphenols and the regulation of  hypertension©

alt

Dr Gelis N. Dimitrios, MD, DDS, PhD, Otorhinolaryngologist, with special interest in Medical nutrition, Supplementary Medicine, Environmental Medicine, Vitamine D, Red wine and Physical Therapies

Damaskinou 45, Korinthos, Greece  tel. 0030274126631,  00306944280764,

e-mail:

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www.gelis.gr,

www.allergopedia.gr,

www.orlpedia.gr,

www.gkelanto.gr,

www.pharmagel.gr 

alt

Ιoan Sorin Stratulat, MD, PhD,                

Professor at:1. University of Medicine and Pharmacy “Gr. T. Popa” Faculty of Medicine/ Dental medicine Iasi,/  Department III Implantology/ Rehabilitation medicine, Phiz. Med. and balneoclimatology,

2.Clinic of Rehabilitation, Physical Medicine and Balneo-climatology, Clinic Hospital C.F. Iasi,  Iasi,Romania.

  1. Alexandru Ioan Cuza University of Iasi, Faculty of Physics, Atmosphere Optics, Spectrsocopy and Lasers Laboratory (LOA-SL)Bd-ul Carol I nr 11, Iasi 700506, Romania

Tel:  +40232201197;  Fax: +40232201150

Web: spectroscopy.phys.uaic.ro

with special interest in vitamin D, Medical Nutrition, Environmental Medicine

alt
Dr Spantideas Anastasios, MD, PhD, Consultant of Internal Medicine, Clinical Pharmacologist, Athens, Greece
alt
Dr Karachalios George, MD, PhD, Consultant Internal Medicine, Clinical Pharmacologist, Athens, Greece
alt

Golas Evangelos, MD, Consultant      Otorhinolaryngologist with special interest in Medical Nutrition, Supplementary Medicine, Environmental Medicine, Vitamin D, Red wine, Ioannina, Greece

www.egolas.gr      This e-mail address is being protected from spambots. You need JavaScript enabled to view it

The most important  risk factor in the development of  a variety of cardiovascular diseases,  coronary artery disease, heart failure including, stroke, and peripheral vascular disease is the hypertension [1].


Hypertension in association with diabetes (DM), renal impairment (RI), and left ventricular hypertrophy (LVH) increases the risk of future cardiovascular events [7]. 


Stroke and coronary artery disease due to atherosclerosis disease  is the most important health issue in modernized society, and hypertension is an important predisposing factor [8, 9]. 


In spite of best available antihypertensive therapies, hypertensive individuals with subclinical target organ damage or cardiovascular risk factors, including left ventricular hypertrophy (LVH), diabetes mellitus, or impaired renal function, are particularly vulnerable to these atherosclerotic complications [10-13]. 


An excessive generation of reactive oxygen species (ROS) due to the increase of the oxidative stress is associated with the pathogenesis of hypertension.. The imbalance between antioxidants defence mechanisms and free radical productions has as a result the increase of blood pressure [1]. 


Accordingly, adjunctive primary preventive strategies, including proper diet modifications, are mandatory in order to decrease the risk of blood pressure establishment.  [7]. 

 

Oxygen and the reactive oxygen species 

One of the most important molecules on Earth is oxygen, mainly because of the biochemical symmetry of oxygenic photosynthesis and aerobic respiration that can maintain homeostasis within our planet's biosphere [2].

 

Reactive oxygen species (ROS) are signaling molecules important in physiological processes including host defense, aging and cellular homeostasis. Increased ROS bioavailability and altered redox signalling (oxidative stress) have been implicated in the onset and/or progression of chronic diseases including hypertension [14].

 

Reactive oxygen species (ROS). ROS are molecules produced by oxygen which play a dual role in biological systems, since they can be either harmful (toxic) or beneficial to living systems. ROS  can be considered a double-edged sword because at moderate concentrations, nitric oxide (NO•), superoxide anion, and related reactive oxygen species play an important role as regulatory mediators in signalling processes [2].


Many of the ROS-mediated responses actually protect the cells against oxidative stress and re-establish "redox homeostasis". On the other hand, overproduction of ROS has the potential to cause damage [2].

 

Increasing evidence from research on several diseases shows that oxidative stress is associated with the pathogenesis of diabetes mellitus, obesity, cancer, cardiovascular diseases, inflammation, ischaemia/reperfusion injury, obstructive sleep apnea, neurodegenerative disorders, hypertension and ageing [2].

 

The term epigenetics refers to the changes in the phenotype and gene expression that occur without alterations in the DNA sequence. There is a rapidly growing body of evidence that epigenetic modifications are involved in the pathological mechanisms of many cardiovascular diseases (CVDs), which intersect with many of the pathways involved in oxidative stress [3].

 

Reactive oxygen species and endothelial dysfunction 

Excessive production of reactive oxygen species reduces nitric oxide bioavailability leading to an endothelial dysfunction , that means an imbalance between endothelium-derived relaxing factors, such as nitric oxide (NO), and contracting factors, such as angiotensin-II and endothelin (ET)-1, favoring the latter. Subsequently it is increased the total peripheral resistance [1].

Vascular remodeling also takes place; both processes lead to hypertension establishment [4].

 

Renal oxidative stress and hypertension 

Although oxidative stress may not be the only cause of hypertension, it amplifies blood pressure elevation in the presence of other pro-hypertensive factors, such as salt loading, activation of the renin-angiotensin-aldosterone system and sympathetic hyperactivity, at least in experimental models [14]. 

 

Renal oxidative stress can be a cause, a consequence or more often a potentiating factor for hypertension. Increased reactive oxygen species (ROS) in the kidney have been reported in multiple models of hypertension and related to renal vasoconstriction and alterations of renal function. Nicotinamide adenine dinucleotide phosphate oxidase is the central source of ROS in the hypertensive kidney but a defective antioxidant system also can contribute [5].

 

Superoxide has been identified as the principal ROS implicated for vascular and tubular dysfunction, but hydrogen peroxide (H2O2) has been implicated in diminishing preglomerular reactivity, and promoting medullary blood flow and pressure-natriuresis in hypertensive animals [5].  

 

Increased renal ROS have been implicated in renal vasoconstriction, renin release, activation of renal afferent nerves, augmented contraction and myogenic responses of afferent arterioles, enhanced tubuloglomerular feedback, dysfunction of glomerular cells and proteinuria [5].

 

Inhibition of ROS with antioxidants, superoxide dismutase mimetics or blockers of the renin-angiotensin-aldosterone system or genetic deletion of one of the components of the signaling cascade often attenuates or delays the onset of hypertension and preserves renal structure and function [5].

 

Novel approaches are required to damper the renal oxidative stress pathways to reduced O2·- rather than H2O2 selectivity and/or to enhance the endogenous antioxidant pathways to renal susceptible subjects to prevent the development and renal damaging effects of hypertension [5].

 

The consequences of hypertension 

Hypertension can cause few symptoms until it reaches the advanced stage and poses serious health problems with lifelong consequences. Hypertensive patients are required to take drugs for life to control the hypertension and prevent complications. Some of these drugs are expensive and may have adverse reactions. Hence, it is timely to examine scientifically, complimentary therapies that are more effective and with minimal undesirable effects [1].

 

The antihypertensive action of antioxidants and polyphenols 

Antioxidant therapies have been evaluated in hypertensive patients, in order to decrease ROS production or increase their scavenging [4].

 

Epidemiological studies have reported a greater reduction in cardiovascular risk and metabolic disorders associated with diets rich in polyphenols [15]. Fruits and vegetables are key foods whose high ingestion is associated with the improvement of numerous pathological conditions, including hypertension. Such health promoting actions have been increasingly ascribed to the antioxidant characteristics of different polyphenols in fruits and vegetables.

 

Consequently, based on this assumption, many beverages and foods rich in polyphenols, grape, red wine, tea, cocoa, and soy products and many of their chemical constituents purified, are being studied both, as antioxidants and antihypertensive agents [1].

 

In this line, polyphenols, widespread antioxidants in fruits, vegetables, and red wine, have demonstrated their beneficial role in prevention and therapy of hypertension, by acting as free radical scavengers, metal chelators,  enzyme expression modulators and regulators of  nitric oxide bioavailability. Polyphenols of red wine,  fruits and vegetables affect endothelial function and as a consequence, blood pressure [6].

 

Polyphenols activate and enhance endothelial nitric oxide synthase (eNOS) expression by several signaling pathways, increase glutathione (GSH), and inhibit ROS-producing enzymes such as NADPH and xanthine oxidases. These pathways lead to improved endothelial function, subsequent normalization of vascular tone, and an overall antihypertensive effect.

 

In practice, diets as Mediterranean and the "French paradox" phenomenon, the light and moderate red wine consumption, supplementation with polyphenols as resveratrol or quercetin, and also experimental and clinical trials applying the mentioned have coincided in the antihypertensive effect of polyphenols, either in prevention or in therapy.


However, further trials are yet needed to fully assess the molecular mechanisms of action and the appearance of adverse reactions, if a more extensive recommendation of polyphenol introduction in diet wants to be made [4].

 

Even when data are not definitive and many questions remain open, the whole evidence is encouraging to start considering diets containing polyphenols that can provide a benefit to hypertensive subjects, and those benefits will be more significant in people that do not have controlled his/her elevated blood pressure [6].

 

Cardiovascular protective effects of red wine polyphenols 

The antioxidant effects of red wine  polyphenols are attributed to the regulation of redox enzymes by reducing reactive oxygen species production from mitochondria, NADPH oxidases and uncoupled endothelial NO synthase in addition to also up-regulating multiple antioxidant enzymes.

 

Although data supporting the effects of red wine polyphenols in reducing oxidative stress are promising, several studies have suggested additional mechanisms in the health benefits of polyphenols. 

 

Polyphenols from red wine increase endothelial NO production leading to endothelium-dependent relaxation in conditions such as hypertension, stroke or the metabolic syndrome.

 

 Numerous molecules contained in red wine, fruits and vegetables can activate sirtuins to increase lifespan and silence metabolic and physiological disturbances associated with endothelial NO dysfunction [15].

 

The beneficial versus toxic effects of alcohol intake 

High red wine intake means increased alcohol use and this is harmful since it is associated with increased incidence of alcoholism, elevated plasma triglycerides, but also with cardiovascular disease, alcoholic fatty liver disease and the development of pancreatitis.

 

Alcohol-induced hypertriglyceridemia is due to increased very-low-density lipoprotein secretion, impaired lipolysis and increased free fatty acid fluxes from adipose tissue to the liver.

 

However, light to moderate alcohol consumption may be associated with decreased plasma triglycerides, probably determined by the type of alcoholic beverage consumed, genetic polymorphisms and lifestyle factors. Nevertheless, patients should be advised to reduce or stop alcohol consumption in case of hypertriglyceridemia [16].

 

The cardioprotective effect of moderate and regular wine consumption in primary prevention has been well documented.

 

Rifler JP, et al (2012), investigated the effect of red wine intake on blood parameters (lipid, anti-oxidant capacity, and erythrocyte membrane potential and fluidity) in selected post myocardial infarct hospitalized patients, in order to evaluate perspectives in secondary prevention, during a cardiac readaptation period.

 

During a period of two-week study  the patients were submitted to a "Western prudent" diet (inspired by the Mediterranean diet) and two groups compared on a drawn basis: patients receiving red wine (250 mL daily) to patients receiving water. They evaluated physical, clinical, and blood parameters on Days 1 and 14. The data showed a positive effect of low red wine consumption on blood parameters (decrease in total cholesterol and LDL; increase in erythrocyte membrane fluidity and antioxidant status) [17].


These  results show that a moderate consumption of red wine even for a short period associated with a "Western prudent" diet improves various blood parameters in lipid and anti-oxidative status in patients with previous coronary ischemic accidents [17].

 

In case that even the moderate use of red wine is not indicated for reasons of alcoholism prevention or liver function protection  the use of condensed organic, natural, sweet, straw red wine (Gkelanto medical red wine) might be useful.. The daily use of 35 ml of Gkelanto medical red wine provides beneficial quantities of red wine polyphenols (resveratrol, siruins, etc) with the less possible use of alcohol.

References 

1. Leong XFRais Mustafa MJaarin K. Nigella sativa and Its Protective Role in Oxidative Stress and Hypertension. Evid Based Complement Alternat Med. 2013;2013:120732. doi: 10.1155/2013/120732. Epub 2013 Mar 7. 

2. Gutowski MKowalczyk S. A study of free radical chemistry: their role and pathophysiological significance. Acta Biochim Pol. 2013 Mar 19. [Epub ahead of print] 

3. Kim GH, Ryan JJ, Archer SL. The Role of Redox Signaling in Epigenetics and Cardiovascular Disease. Antioxid Redox Signal. 2013 Mar 12. [Epub ahead of print] 

4. Rodrigo RGil DMiranda-Merchak AKalantzidis G. Antihypertensive role of polyphenols. Adv Clin Chem. 2012;58:225-54. 

5. Araujo MWilcox CS. Oxidative stress in hypertension: role of the kidney. Antioxid Redox Signal. 2013 Mar 9. [Epub ahead of print] 

6. Galleano M, Pechanova O, Fraga CG. Hypertension, nitric oxide, oxidants, and dietary plant polyphenols. Curr Pharm Biotechnol. 2010 Dec;11(8):837-48. 

7. Woo KSYip TWChook PKwong SKSzeto CCLi JKYu AWCheng WKChan TYFung KPLeung PC. Cardiovascular Protective Effects of Adjunctive Alternative Medicine (Salvia miltiorrhiza and Pueraria lobata) in High-Risk Hypertension. Evid Based Complement Alternat Med. 2013;2013:132912. doi: 10.1155/2013/132912. Epub 2013 Mar 7.

 8. Murray CJL, Lopez AD. Mortality by cause for eight regions of the world: Global Burden of Disease Study. The Lancet. 1997;349(9061):1269–1276. [PubMed] 

9. Kearney PM, Whelton M, Reynolds K, Muntner P, Whelton PK, He J. Global burden of hypertension: analysis of worldwide data. The Lancet. 2005;365(9455):217–223. [PubMed] 

10. Koren MJ, Devereux RB, Casale PN, Savage DD, Laragh JH. Relation of left ventricular mass and geometry to morbidity and mortality in uncomplicated essential hypertension. Annals of Internal Medicine. 1991;114(5):345–352. [PubMed] 

11. National Kidney Foundation. K/DOQI clinical practice guidelines on hypertension and antihypertensive agents in chronic kidney disease. American Journal of Kidney Diseases. 2004;43(supplement 1):S1–S290. [PubMed] 

12. Almgren T, Wilhelmsen L, Samuelsson O, Himmelmann A, Rosengren A, Andersson OK. Diabetes in treated hypertension is common and carries a high cardiovascular risk: results from a 28-year follow-up. Journal of Hypertension. 2007;25(6):1311–1317. [PubMed] 

13. Mancia G, de Backer G, Dominiczak A, et al. 2007 Guidelines for the management of arterial hypertension: the task force for the management of arterial hypertension of the European Society of Hypertension (ESH) and of the European Society of Cardiology (ESC) European Heart Journal. 2007;28:1462–1536. [PubMed] 

14. Montezano ATouyz RM. Reactive oxygen species, vascular Noxs and hypertension: Focus on translational and clinical research. Antioxid Redox Signal. 2013 Apr 22. [Epub ahead of print] 

15. Andriantsitohaina RAuger CChataigneau TÉtienne-Selloum NLi HMartínez MCSchini-Kerth VBLaher I. Molecular mechanisms of the cardiovascular protective effects of polyphenols. Br J Nutr. 2012 Nov 14;108(9):1532-49. doi: 10.1017/S0007114512003406. Epub 2012 Aug 31. 

16. Klop BRego ATCabezas MC. Alcohol and plasma triglycerides. Curr Opin Lipidol. 2013 Mar 17. [Epub ahead of print] 

17. Rifler JPLorcerie FDurand PDelmas DRagot KLimagne EMazué FRiedinger JMd'Athis PHudelot BProst MLizard GLatruffe N. A moderate red wine intake improves blood lipid parameters and erythrocytes membrane fluidity in post myocardial infarct patients. Mol Nutr Food Res. 2012 Feb;56(2):345-51. doi: 10.1002/mnfr.760.

Last Updated (Friday, 16 August 2013 22:05)

 
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