China
Africa
Explore chapters and articles related to this topic
Flaxseed and L-Arginine, and Omega-3 Fatty Acids, per se, in Treatment of Hypertension and Sickle Cell Disease
Published in Robert Fried, Richard M. Carlton, Flaxseed, 2023
Robert Fried, Richard M. Carlton
Asymmetric dimethylarginine (ADMA) is an analogue of L-arginine that is a naturally occurring product of metabolism found in human circulation. Elevated levels of ADMA inhibit NO formation, impairing endothelial function and thus promoting atherosclerosis. ADMA levels are increased in people with hypercholesterolemia, atherosclerosis, hypertension, chronic heart failure, diabetes mellitus and chronic renal failure. A number of studies have reported ADMA as a novel risk marker of cardiovascular disease.
Selected Functional Foods That Combat the Effects of Hyperglycemia and Chronic Inflammation
Published in Robert Fried, Richard M. Carlton, Type 2 Diabetes, 2018
Robert Fried, Richard M. Carlton
Furthermore, in diabetes, increased plasma levels of asymmetric dimethylarginine (ADMA), an endogenous competitive inhibitor of NO synthase, is also a known hyperglycemia-induced impairment factor of the NO pathway (Lin, Ito, Asagami et al. 2002). In addition, decreased NOS activity and decreased production of NO from l-arginine, as well as increased arginase activity (which leads to decreased l-arginine bioavailability and thus decreased NO synthesis), are other disrupted pathways in NO homeostasis in diabetic conditions (Romero, Caldwell, and Caldwell. 2006). Since activation of NOS is regulated also by insulin, and the Akt signaling pathway, impaired insulin secretion and insulin resistance due to diabetes could affect NO synthesis (Vincent, Montagnani, and Quon. 2003).
The Cardiovascular System
Published in Pritam S. Sahota, James A. Popp, Jerry F. Hardisty, Chirukandath Gopinath, Page R. Bouchard, Toxicologic Pathology, 2018
Calvert Louden, David Brott, Chidozie J. Amuzie, Bindu Bennet, Ronnie Chamanza
VEGF and asymmetric dimethylarginine (ADMA) are secretory products from EC as well as other cells in the body that affect endothelial and smooth muscle cell function, and therefore could have utility as diagnostic markers of vascular injury. The biochemical pharmacology implicates VEGF activation of vascular tyrosine kinase receptors to be the cause of vasodilation, and consequently hypotension through the NO pathway (Bussolati et al. 2001; Hennequin et al. 1999).
The effects of melatonin against atherosclerosis-induced endothelial dysfunction and inflammation in hypercholesterolemic rats
Published in Archives of Physiology and Biochemistry, 2023
Dilşad Sezgin, Gülnur Aslan, Kazım Sahin, Mehmet Tuzcu, Necip İlhan, Engin Sahna
Asymmetric dimethylarginine (ADMA), endothelial nitric oxide synthase (eNOS) inhibitor, reduces vasodilator nitric oxide (NO) levels. Increased ADMA levels and endothelial dysfunction caused by ox-LDL in hypercholesterolaemia are the first and most important indicators of atherosclerosis (Landim et al.2013). ADMA is metabolised by the activity of DDAH, which is known to be a highly oxidation-sensitive enzyme. dimethylarginine dimethylaminohydrolase (DDAH) activity is accepted as a major determinant of endogenous ADMA concentration (Sibal et al.2010). Vaspin, an adipocytokine with a regulatory role in glucose and lipid metabolism, reduces the progression of atherosclerosis (Lin et al.2016). Visfatin is a reagent of inflammation and endothelial dysfunction and participates in early pro-atherosclerotic events via increasing the accumulation of triglycerides in adipocytes and the production of triglycerides from glucose (Dahl et al.2007). Signal transducer and activator of transcription 3 (STAT-3) is an important transcription factor that regulates proinflammatory genes in endothelial cells (Mattagajasingh et al.2012). All these biochemical markers are reported to play roles in NO metabolism (McCormick et al.2011, Jung et al.2012, Akbarian et al.2018).
The effect of hemodialysis on ocular changes in patients with the end-stage renal disease
Published in Renal Failure, 2019
Guijiang Sun, Rui Hao, Longli Zhang, Xueying Shi, Kaiwen Hei, Lijie Dong, Fang Wei, Aili Jiang, Bo Li, Xiaorong Li, Yifeng Ke
The mechanism of the dialysis-associated vasodilatation is not clear. Usually, endothelium-dependent vasodilatation was thought to be the major vasodilatation mechanism in ESDR patients [19]. Endothelium-dependent dilatation in response to flow-mediated shear stress is impaired in the resistant vasculature from patients with ESRD and finally result in contraction of resistance vasculature due to blunted blood flow and the lack of nitric oxide (NO) contribution [20]. However, dilatation of the retinal microvasculature after dialysis is thought to occur secondary to the release of vasoactive factors, such as nitric oxide, nitrotyrosine, Asymmetric dimethylarginine (ADMA), heat shock proteins, in response to the reduced intravascular volume [21]. For example, asymmetric dimethylarginine, an inhibitor of nitric oxide synthase, accumulates in renal failure [22], The elevated levels of ADMA would decrease NO production. However, it was removed by dialysis, resulting in enhanced nitric oxide production and consequent vasodilatation. And so did the nitrotyrosine [20].
Asymmetric dimethylarginine compartmental behavior during high-flux hemodialysis
Published in Renal Failure, 2020
Qiuna Du, Jiayuan Gao, Renhua Lu, Yun Jin, Yanfang Zou, Chen Yu, Yucheng Yan
Cardiovascular disease (CVD) is the leading cause of mortality in end-stage renal disease (ESRD) patients with an incidence of 10–20 times higher than that in the general population [1]. Traditional risk factors, including diabetes mellitus, hypertension, obesity, dyslipidemia, and smoking, do not completely account for the excess CVD in this patient group. Indeed, other factors, including the accumulation of uremic toxins, such as asymmetric dimethylarginine (ADMA), have emerged as major risk factors in patients with ESRD [2–4].