The effect of pharmacological treatment on ADMA in patients with heart failure

Riccioni, Graziano; Speranza, Lorenza; Scotti, Luca; Bucciarelli, Valentina; Ilio, E. Di; D’Orazio, Nicolantonio; Pesce, Mirko; Aceto, Antonio; Sorrenti, Valeria; Frigiola, Alessandro; Bucciarelli, Tonino

doi:10.2741/e334

Cited by 9 publications

(8 citation statements)

References 20 publications

(22 reference statements)

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“…This proinflammatory effect, together with the indirect effects of SDMA on NO synthesis, and the relationship of SDMA to renal function are thought to be possible mechanisms by which SDMA and CVD may be linked (34). Although no evidence exists as yet that SDMA inhibits NO synthase, it may interfere with arginine transport into the cells and, therefore, NO production could be reduced indirectly as already shown by others (35)(36)(37). The high SDMA concentrations in renal patients with CAD could indicate such an increase in vascular tone (38,39).…”

Section: Discussionmentioning

confidence: 87%

Physical exercise reduces synthesis of ADMA SDMA and L-Arg

Riccioni¹

2015

Front Biosci

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Increased levels of asymmetric dimethylarginine (ADMA), symmetric dimethylarginine (SDMA) and low plasma level of L-arginine (L-ARG) are all conditions likely to decrease nitric oxide (NO) production. Aim of this study is to evaluate ADMA, SDMA, and L-ARG plasmatic levels before and after physical exercise in patients with coronary artery disease (CAD). We studied 30 patient with mean age 52 + 4.5 years. After inclusion in the study, before the execution of physical exercise, heparinized blood sample was drawn from an indwelling arterial line for determination of ADMA, L-ARG and SDMA (baseline values). Subsequently a blood sample was drawn after the physical exercise. The mean plasma concentrations of ADMA (0.68 + 0.06 vs 0.48 + 0.05 µmol/L) and SDMA (0.45 + 0.03 vs 0.30 + 0.03 µmol/L) were significantly lower after physical exercise in comparison to baseline value, while L-ARG mean levels were increased (44.20 + 10.5 vs 74.13 + 11.2 µmol/L). Physical exercise has a beneficial effect by reducing plasmatic ADMA and SDMA levels, and increasing L-ARG substrate for endothelial NO.

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Section: Discussionmentioning

confidence: 87%

Physical exercise reduces synthesis of ADMA SDMA and L-Arg

Riccioni¹

2015

Front Biosci

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“…Urinary ADMA and creatinine levels were determined as previously reported 41‐43 . The HPLC apparatus consisted of a Jasco PU‐2080 chromatographic pump and a Jasco MD‐2010 Plus absorbance detector.…”

Section: Methodsmentioning

confidence: 99%

Effect of high‐altitude trekking on blood pressure and on asymmetric dimethylarginine and isoprostane production: Results from a Mount Ararat expedition

Verratti

Ferrante

Soranna

et al. 2020

J of Clinical Hypertension

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The study aimed at exploring the mechanisms behind blood pressure and heart rate changes upon acute altitude exposure utilizing urinary excretion of biochemical factors involved in cardiovascular regulation. The study was conducted on 12 lowlander native male mountain climbers, living at sea level, exposed to altitudes ranging from 1800 to 5147 m above sea level over 4 days, during their ascent to Mount Ararat (Turkey). Blood pressure (measured by oscillometric method), heart rate, and blood oxygen saturation (SpO2) were recorded at rest (on awakening before food intake), in hypoxic conditions at 4200 m and at sea level before and after the altitude expedition. In the same study conditions (ie before‐during‐after the expedition), first‐voided urinary samples were collected and assayed for 8‐iso‐prostaglandin F2α (8‐iso‐PGF2α) and asymmetric dimethylarginine (ADMA) determination. Heart rate, and systolic and diastolic blood pressures were higher (P < .05) at high altitude than at the sea level. Furthermore, both urinary 8‐iso‐PGF2α and ADMA were significantly elevated (P < .01) at high altitude and returned to normal levels soon after returning to sea level. A 4‐day exposure to high‐altitude hypoxia induced a temporary increase in blood pressure and heart rate, confirming previous findings. Blood pressure increase at high altitude was associated with significantly enhanced production of biochemical mediators such as 8‐iso‐PGF2α, catecholamines, and ADMA, although we could not demonstrate a direct link between these parallel significant changes probably due to the forcefully limited sample size of our study, carried out in challenging environmental conditions at very high altitude.

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“…There is not only evidence that these molecules modulate NO synthesis in vivo , but also that this pathway has a primary role in the pathogenesis of disease. In addition, a degree of tissue/cell specificity of the enzymes controlling methylarginine levels, along with potential for playing a key homeostatic role in NO synthesis, makes this pathway an attractive target for therapeutic intervention [22,23]. There have been a series of in vitro , in vivo , and clinical investigations designed to characterize the pathological role of the endogenous methylarginines in human health and disease (Table 1).…”

Section: Adma In Oxidative Stress Inflammation and Cardiovascular DImentioning

confidence: 99%

“…ADMA has been suggested as a novel independent risk factor for endothelial dysfunction and coronary heart disease. Increased plasma levels of ADMA have been documented in several conditions that are characterized by endothelial dysfunction, including hypertension, hypercholesterolemia, hyperglycemia, renal failure and tobacco exposure (Figure 2) [22,29,36]. …”

Section: Adma In Oxidative Stress Inflammation and Cardiovascular DImentioning

confidence: 99%

Biological Functional Relevance of Asymmetric Dimethylarginine (ADMA) in Cardiovascular Disease

Franceschelli

Ferrone

Pesce

et al. 2013

IJMS

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There is growing evidence that increased levels of the endogenous NO synthase inhibitor asymmetric dimethylarginine (ADMA) may contribute to endothelial dysfunction. Studies in animal models as well as in humans have suggested that the increase in ADMA occurs at a time when vascular disease has not yet become clinically evident. ADMA competitively inhibits NO elaboration by displacing l-arginine from NO synthase. In a concentration-dependent manner, it thereby interferes not only with endothelium-dependent, NO-mediated vasodilation, but also with other biological functions exerted by NO. The upshot may be a pro-atherogenic state. Recently, several studies have investigated the effect of various therapeutical interventions on ADMA plasma concentrations.

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The effect of pharmacological treatment on ADMA in patients with heart failure

Cited by 9 publications

References 20 publications

Physical exercise reduces synthesis of ADMA SDMA and L-Arg

Physical exercise reduces synthesis of ADMA SDMA and L-Arg

Effect of high‐altitude trekking on blood pressure and on asymmetric dimethylarginine and isoprostane production: Results from a Mount Ararat expedition

Biological Functional Relevance of Asymmetric Dimethylarginine (ADMA) in Cardiovascular Disease

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