Where To Buy Arginine Cardio [UPD]
There are plenty of powerful new drugs to help prevent and treat chronic health problems. But we also know that certain nutrients may help, as well. Take arginine, for example. Arginine has gotten lots of attention lately for its potential heart benefits. That's important because, today, more than 85 million Americans have some form of cardiovascular disease.
where to buy arginine cardio
Deficiencies of arginine are rare. It's abundant in many different types of foods, and your body can also make it. Arginine-rich foods include red meat, fish, poultry, wheat germ, grains, nuts and seeds, and dairy products. But what does arginine do for the heart, and are there potential side effects?
Some evidence shows that arginine may help improve blood flow in the arteries of the heart. That may improve symptoms of clogged arteries, chest pain or angina, and coronary artery disease. However, there currently is no data on how the long-term use of arginine affects cholesterol or heart health.
There are other potential health benefits with arginine, such as possible reduction of blood pressure in some people and improved walking distance in patients with intermittent leg cramping and weakness known as intermittent claudication. However, the scientific studies are not conclusive enough for experts to make any firm recommendations.
In clinical trials, arginine has been used safely with minor side effects for up to three months. Possible side effects include abdominal pain and bloating, diarrhea, and gout. It may also cause a worsening of breathing in people with asthma.
L-arginine and its derivatives, asymmetric and symmetric dimethylarginine (ADMA and SDMA) and L-homoarginine, have emerged as cardiovascular biomarkers linked to cardiovascular outcomes and various metabolic and functional pathways such as NO-mediated endothelial function. Cellular uptake and efflux of L-arginine and its derivatives are facilitated by transport proteins. In this respect the cationic amino acid transporters CAT1 and CAT2 (SLC7A1 and SLC7A2) and the system y+L amino acid transporters (SLC7A6 and SLC7A7) have been most extensively investigated, so far, but the number of transporters shown to mediate the transport of L-arginine and its derivatives is constantly increasing. In the present review we assess the growing body of evidence regarding the function, expression, and clinical relevance of these transporters and their possible relation to cardiovascular diseases.
Background: Oxidative/nitrosative stress and endothelial dysfunction are hypothesized to be central to cancer therapeutics-related cardiac dysfunction (CTRCD). However, the relationship between circulating arginine-nitric oxide (NO) metabolites and CTRCD remains unstudied.
Objectives: This study sought to examine the relationship between arginine-NO metabolites and CTRCD in a prospective cohort of 170 breast cancer patients treated with doxorubicin with or without trastuzumab.
Methods: Plasma levels of arginine, citrulline, ornithine, asymmetric dimethylarginine (ADMA), symmetric dimethylarginine (SDMA), and N-monomethylarginine (MMA) were quantified at baseline, 1 month, and 2 months after doxorubicin initiation. Determinants of baseline biomarker levels were identified using multivariable linear regression, and Cox regression defined the association between baseline levels and 1- or 2-month biomarker changes and CTRCD rate in 139 participants with quantitated echocardiograms at all time points.
Conclusions: In breast cancer patients undergoing doxorubicin therapy, early alterations in arginine-NO metabolite levels occurred, and early biomarker changes were associated with a greater CTRCD rate. Our findings highlight the potential mechanistic and translational relevance of this pathway to CTRCD.
Together, these functions make NO a significant endogenous anti-atherosclerotic molecule. A reduction in NO can result in endothelial dysfunction and in an increased risk for cardiovascular disease. Endothelial dysfunction precedes overt atherosclerotic disease. Previous studies have shown endothelial dysfunction to predict the presence of cardiovascular disease and future cardiovascular events [11, 12].
In 1992, Vallance and co-workers reported that asymmetric dimethylarginine (ADMA) is a naturally occurring endogenous inhibitor of nitric oxide (NO) synthase [13]. ADMA reduces NO production and consequently could thus lead to endothelial dysfunction and cardiovascular events. An increased understanding of the pathophysiology of atherosclerosis, particularly of the central role of endothelial dysfunction, has led to the emergence of plasma ADMA as a putative cardiovascular risk marker.
Overview of pathways of synthesis and metabolism of ADMA. Methylation of arginine residues within peptides occurs through N-methyltransferases, protein arginine N-methyltransferase-1 (PRMT-1). S-adenosylmethionine (SAM) is the methyl donor, changing to S-adenosylhomocysteine (SAH). Proteolytic breakdown of the proteins leads to the generation of ADMA and N-monomethyl-L-arginine (L-NMMA) within cells, and is detectable in the circulation. ADMA is an inhibitor of endothelial nitric oxide synthase (eNOS) by competing with its substrate L-arginine thus impairing nitric oxide (NO) production, thus leading to endothelial dysfunction and subsequently atherosclerosis. ADMA is eliminated partly via urinary excretion but mainly via metabolism by the enzyme dimethylarginine dimethylaminohydrolase (DDAH) to citrulline and dimethylamine.
DDAH activity has been found in kidney, pancreas, liver, brain and aorta with immunoexpression also in neutrophils and macrophages [33, 34]. Inhibition of DDAH causes gradual vasoconstriction which is reversed by L-arginine [35]. There are two isoforms of DDAH, DDAH-1 and DDAH-2. DDAH-1 is usually found in tissues expressing neuronal NOS while DDAH-2 is predominantly found in tissues containing the endothelial isoform of NOS [36]. Increased plasma levels of glucose, oxidized LDL and homocysteine are associated with decreased levels of DDAH. Furthermore, some conventional cardiovascular risk factors may reduce DDAH activity by increasing oxidative stress [37-40]. Pharmacological inhibition of DDAH increases ADMA concentrations and reduces NO production [41].
Perticone and colleagues studied serum ADMA levels and endothelial function in people with essential hypertension [55]. People with hypertension had impaired brachial artery FMD and increased ADMA levels. These measures were inversely correlated with ADMA levels independently accounting for 34% of the interindividual variability in peak flow-mediated dilatation. Infusion of L-arginine improved the endothelial function.
In the young Finns study involving 2096 white adults, of age 24-39 years, plasma ADMA levels and brachial artery FMD was measured along with other conventional cardiovascular risk factors. There was an inverse correlation between ADMA and FMD. This inverse association between ADMA and FMD remained significant in a multivariate regression model adjusted for age, sex, conventional cardiovascular risk factors, estimated glomerular filtration rate and baseline brachial artery diameter [57].
ADMA has been found to modulate coronary endothelial function [60] and promotes coronary spasm in small studies [61]. However, in a randomized, double-blind trial in 289 patients with coronary artery disease, ADMA, L-arginine and coronary endothelial function as assessed by the coronary artery response to local acetylcholine infusion were measured [62]. No correlation between coronary endothelial function and ADMA levels was found. In another study, coronary endothelial dysfunction was shown to be independently associated with erectile dysfunction and plasma ADMA concentration in men with early coronary atherosclerosis [63].
In a prospective trial of 225 patients undergoing haemodialysis, age and ADMA levels were the strongest predictors of cardiovascular events and mortality after a median follow- up of 33 months [77]. The Coronary Artery Risk Determination investigating the Influence of ADMA Concentration (CARDIAC) study included 800 people with and without established coronary artery disease (CAD). The plasma ADMA concentration was 20% higher in the presence of established CAD (stable angina or MI) and the ADMA levels increased with increasing number of cardiovascular risk factors. The risk of CAD increased by more than two-fold for every 1 µmol/l increase in plasma ADMA [78]. In a prospective, nested, case-control study of middle-aged men from Finland, Valkonen and colleagues reported a 3.9 fold increased risk of acute coronary events in subjects with highest quartile of ADMA compared to other quartiles [23].
Lu and colleagues followed-up 153 people with stable angina undergoing percutaneous coronary intervention for a duration of 16 months during which time major cardiovascular events occurred in 51 patients. An increased risk of cardiovascular events was noted with increasing levels of ADMA which was independent of any confounding factors in a multi-factorial Cox regression analysis [22].
In the Ludwigshafen Risk and Cardiovascular Health (LURIC) study, 2543 people with angiographically documented CAD and 695 with no CAD were followed-up for 5.5 years [24]. Increased all-cause mortality and death due to cardiovascular causes were noted in the second, third and fourth quarters of ADMA when compared to the lowest quarter (hazard ratio of 1.09, 1.40 and 2.04 respectively). However, the predictive value of ADMA was not statistically significant in the subgroup of patients without angiographically proven CAD [24].
In the AtheroGene study, baseline serum concentrations of ADMA were studied in 1874 consecutive patients with CAD who were then followed-up for 2.61.2 years. The primary end-point was death from cardiovascular causes or non-fatal myocardial infarction. The median ADMA levels in patients who subsequently experienced the primary end-point was significantly higher than in patients who did not reach the primary end-point. The hazard ratio for the primary end-point was 2.48 times higher in patients whose ADMA was above the highest tertile compared to those in who ADMA was below the lowest tertile [79]. 041b061a72