Asymmetric Dimethylarginine (ADMA): A Promising Biomarker for Cardiovascular Disease?

Bouras, Georgios; Deftereos, Spyridon; Tousoulis, Dimitrios; Γιαννόπουλος, Γεώργιος; Chatzis, Georgios; Tsounis, Dimitrios; Cleman, Michael; Stefanadis, Christodoulos

doi:10.2174/1568026611313020007

Cited by 99 publications

(61 citation statements)

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“…1,[73][74][75][76][77] Thus, incremental NO reduction results in incremental ET-1 release, which contributes to several cardiovascular diseases. 1,77 Importantly, accurate modeling of the conditions required for endogenous NO-mediated decreased ET-1 release will allow further relevant investigation into potential interventions that reverse/ prevent the disruption of this negative regulatory pathway and, thus, eventual therapeutic modalities.…”

Section: Discussionmentioning

confidence: 99%

Nitric Oxide Inhibition of Endothelin-1 Release in the Vasculature

Rapoport

2014

Hypertension

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A key function of endothelial derived nitric oxide (NO) is to limit the constrictor capacity of endothelin (ET)-1.1,2 Thus, an imbalance between NO and ET-1 can result in ET-1-dependent increased vascular tone.1 Indeed, the importance of sustained, NO inhibition of the ET-1 drive to increase tone is exemplified in vivo by the rapid, ET-1-mediated arterial pressure elevation after acute NO synthase (NOS) inhibition. Moreover, the ET-1 pressor effect after NOS inhibition is independent of other pressor systems and, thus, reflects the relative importance of NO suppression of this ET-1 drive.2 Two, nonmutually exclusive mechanisms thought to underlie the ET-1 dependency of the increased vascular tone responsible for the NOS inhibitor-induced pressure elevation are (1) NO inhibition of constriction to endogenously released ET-1.1,2 This mechanism is essentially supported by demonstrations that NOS inhibitor enhanced the constrictor effects of exogenous ET-1 in several in vivo and ex vivo preparations. 3-14Thus, an assumption underlying these observations is that the constrictor actions of exogenous and endogenous ET-1 are similarly affected by NO; (2) NO inhibition of ET-1 release. 1,2Although the detailed mechanism underlying the NO inhibition of acute ET-1 release has not been clearly established, possibilities include decreased conversion of the immediate precursor to ET-1, big ET-1, to ET-1 15 and inhibition of pathways involved in the exocytosis of Weibel-Palade bodies, 16 endothelial granules that store ET-1. 17 However, it should be noted that in vivo findings that actually demonstrate the fundamental phenomenon of NO inhibition of ET-1 release are generally lacking.2 Thus, studies purported to demonstrate NO inhibition of ET-1 release have relied largely on isolated vessels and cultured endothelium, as described herein.This review assessed these in vitro findings, with a specific focus toward elucidating the mechanism underlying the NO-mediated negative regulation of ET-1-dependent increased arterial pressure, as demonstrated after acute NOS inhibitor in vivo.2 Findings referred to are mainly those of ET-1 release rather than contractility (eg, those in which ET receptor antagonist prevented the NOS inhibitor-induced decreased flow/increased pressure/tension). 12,18-25 The rationale for this emphasis is that findings based on contractility could reflect NOS inhibitor enhancement of ET-1 constriction rather than increased ET-1 release. Furthermore, we also focus on whether laminar shear stress influences the manifestation of NO inhibition of ET-1 release. That is, the endothelium of arteries that are anatomically linear is subjected to high levels of shear stress while, for example, at bifurcated arterial locations is subjected to low levels of shear stress, regions associated with atherosclerosis. 26 Acute NOS Inhibition/No Donors and ET-1 Release ArteriesIn rat heart perfused at constant flow, increased amounts of ET-1 were detected in the coronary effluent of samples collected for the final 5 to 15 minutes ...

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Section: Discussionmentioning

confidence: 99%

Nitric Oxide Inhibition of Endothelin-1 Release in the Vasculature

Rapoport

2014

Hypertension

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“…This has been explained for the vasoconstriction and endothelial injury. A positive correlation of ADMA level and HHcy has been reported [2]. An increase in ADMA has been associated with approximately 4 fold increase in the risk for atherosclerosis [3].…”

Section: Role Of Hyperhomocysteinemia In Dementiamentioning

confidence: 88%

Supplementation of Pyridoxine, Folate and Cobalamine in Older People: An Analysis on their Effect on Hyperhomocysteinemia and Dementia

2017

International Journal of Clinical Chemistry and Laboratory Medi

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“…FGF-23 elevation plays a role in the pathogenesis of endothelial dysfunction [14,43], atherosclerosis [13], and left ventricular hypertrophy [44]. On the other hand, ADMA is an endogenous inhibitor of nitric oxide production and a promising biomarker for cardiovascular diseases [45]. To our knowledge, very few studies have reported the effect of TRT on ADMA levels in the literature.…”

Section: Discussionmentioning

confidence: 99%

Wpływ testosteronowej terapii zastępczej na stężenia witaminy D i FGF-23 w hipogonadyzmie wrodzonym

Haymana¹,

Sönmez²,

Aydoğdu³

et al. 2017

Endokrynologia Polska

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Introduction: Patients with hypogonadism are at increased risk of cardiac and metabolic diseases and osteoporosis. Vitamin D and fibroblast growth factor-23 (FGF-23) play a role in the regulation of bone mineral metabolism and endothelial functions. Low vitamin D levels are reported in hypogonadism, while there is no data about the effect of testosterone replacement therapy (TRT). We investigated the effect of TRT on vitamin D and FGF-23 levels along with endothelial functions and insulin resistance in hypogonadal patients. Material and methods:Patients with congenital hypogonadotrophic hypogonadism (CHH) (n = 32, age 20.6 ± 1.58 years) were enrolled. TRT was implemented in transdermal form. The demographic parameters, FGF-23, 25(OH)D3, asymmetric dimethylarginine (ADMA), and homeostatic model assessment of insulin resistance (HOMA-IR) levels, were measured both before and after TRT. Results: After a follow-up period of 3.63 ± 1.33 months, ADMA and FGF-23 levels were significantly increased (p = 0.03 and p = 0.005 respectively), while 25(OH)D3 and HOMA-IR index were not significantly changed. The body mass index and waist circumference levels of the patients were also increased (p < 0.001 and p = 0.02) along with a significant decrease in the HDL cholesterol levels (p = 0.006). Conclusions:The results show that short-term TRT increases plasma FGF-23 and ADMA levels but does not alter the vitamin D levels in young, treatment naive patients with CHH. Whether this is an early implication of TRT-related adverse effects in this very young and treatment naïve population of CHH is not clear. Future prospective studies are required to find out the long-term effects of TRT on cardiometabolic morbidity and mortality in this specific population. (Endokrynol Pol 2017; 68 (3): 311-316)

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Asymmetric Dimethylarginine (ADMA): A Promising Biomarker for Cardiovascular Disease?

Cited by 99 publications

References 0 publications

Nitric Oxide Inhibition of Endothelin-1 Release in the Vasculature

Nitric Oxide Inhibition of Endothelin-1 Release in the Vasculature

Supplementation of Pyridoxine, Folate and Cobalamine in Older People: An Analysis on their Effect on Hyperhomocysteinemia and Dementia

Wpływ testosteronowej terapii zastępczej na stężenia witaminy D i FGF-23 w hipogonadyzmie wrodzonym

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