Cardiovascular dairy products. In this review, the focus is

Cardiovascular disease (CVD) is one of the leading causes of morbidity and mortality around the world today due to largely a combination of lifestyle patterns such as diet, physical inactivity, smoking, etc (Bonow et al., 2011). These lifestyle patterns combine to produce certain symptoms such as hypertension that puts individuals at higher risk for stroke, CVD, and other chronic diseases. Hypertension, or high blood pressure, is a symptom that can be managed through nutrition, more specifically, by following the Dietary Approaches to Stop Hypertension (DASH) diet. This diet includes eating a lot of fruits, vegetables and reducing fat and sodium intake overall. The DASH diet also includes a protein that lowers blood pressure due to the amino acid arginine (Vasdev & Gill, 2008). The amino acid, L-arginine helps reduce hypertension by vasodilation via acting as the main substrate for endothelium-specific isoform of nitric oxide (NO) synthase (eNOS) (Gokce, 2004). Once NO is produced, it will activate guanylate cyclase to make cyclic GMP. GMP assists in relaxation and vasodilation of vessels (Vasdev & Gill, 2008).  Therefore, supplementing protein, or L-arginine, in the diet of hypertensive patients, can help reduce the risk of CVD (Gokce, 2004). This review paper will discuss the cellular mechanisms, and the correlation involved with L-arginine and hypertension reduction.

 

 

 

 

 

 

 

Introduction

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Worldwide, approximately six hundred million people are affected by hypertension, a main risk factor of CVD. Hypertension can be determined by genetics, but diet tends to have a bigger influence. To reduce or manage the effects of hypertension, patients are advised to follow the DASH diet. As mentioned previously, the DASH diet consists of eating a lot of healthy, organic foods such as fruits, vegetables and low-fat meat and dairy products. In this review, the focus is on protein, or the amino acid L-arginine (Vasdev & Gill, 2008). It has been shown in many studies that protein, replacing carbohydrates, in a DASH diet, has an inverse relationship with blood pressure which means that dietary protein supplementation reduces and treats hypertension. It is believed that proteins, specifically the amino acids cysteine, glutamate, arginine, leucine, taurine, tryptophan, assist in reducing hypertension through influencing the processes of insulin resistance, advanced glycation, oxidative stress, etc. The mechanisms behind these processes remain unclear in some parts. However, L-arginine shows major influence on hypertension (Bazzano et al., 2013).

L-arginine supplemented diet can reduce hypertension, through vasodilation of the vessels by increasing NO production via eNOS which causes the vessels to vasodilate by generating cyclic (c)GMP (Vasdev & Gill, 2008; Gokce, 2004). NO activity is very important in hypertension because lack of NO production can cause endothelial dysfunction. Several longitudinal studies display that the loss of proper endothelial function can cause complications in CVD, and other cerebral, renal function as well. L-arginine plays a key role in controlling endothelial homeostasis in CVD or in other words, NO causes vasodilation which reduces blood pressure (Gokce, 2004). Therefore, the importance lies in incorporating arginine-supplemented diets to patients with hypertension and CVD. It is very important to treat hypertension as early as possible because if adverse reactions, such as myocardial infarction, which causes, the cardiac tissue damage is irreversible even with protein supplementation. This review article will focus on how NO production ultimately reduces hypertension through the use of L-arginine and the processes involved with it.

L-arginine is a semi-essential amino acid that is made by the body in the kidney, and liver through the urea cycle. However, it can also be taken through diet in foods such as soy, fish, beans, lentils, and nuts (Vasdev & Gill, 2008). Supplementation of L-arginine is necessary for conditions like malnutrition, infections, sepsis, and CVD. For cardiovascular diseases, L-arginine can be administered through the DASH diet. The normal L-arginine concentration, ~ 3 ?mol/L, in the body is not sufficient to saturate eNOS. Due to this, supplementation proves to be effective in stimulating the eNOS process (Alvares et al, 2012).

The function of L-arginine in the physiological process includes acting as a substrate for initiating the eNOS mechanism. As mentioned in the abstract, eNOS stands for endothelium-specific isoform of nitric oxide synthase (eNOS). This process of eNOS is associated with multiple activities, and multiple proteins within the body to regulate sub-cellular localization, catalytic activities through phosphorylation, nitrosylation, and etc (Dudzinski & Michel, 2007). Besides these functions, eNOS is involved in vasodilation. One of the proteins that help this localized regulation of blood vessel walls is L-arginine. By acting as the substrate, it activates the eNOS process to make nitric oxide. NO synthesis occurs through the catalyzation of five electron oxidation of L-arginine to L-citrulline by eNOS with the help of co-factors such as tetrahydrobiopterin, flavin adenine dinucleotide, flavin mononucleotide, heme and NADPH (Wu & Meininger, 2000; Vasdev & Gill, 2008). When this catalyzation takes place, NO is produced as a result. The vasodilation of the vessels then takes place due to NO and cGMP. The NO synthesis will activate the guanylyl cyclase to generate cGMP, which will cause relaxation of the vascular smooth muscle cells (Wu & Meininger, 2000). When vasodilation occurs by relaxing the smooth muscle cells, the vascular resistance decreases, and improves blood flow. The mechanism involved include cGMP in the vascular smooth muscle activating potassium, (K), channels of the membrane. By activating the K channels, K efflux takes place and hyperpolarization occurs. The hyperpolarization inactivates the L-type voltage-gated calcium channels and causes relaxation of the vessels (Stoen et al.,2001; Archer et al., 1994).