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L-Arginine Thread - Consolidating all its Info

L-Arginine Thread - Consolidating all its Info

Information on L-Arg is scattered in disparate posts so I find it quite tedious to put together the information to form a coherent big picture.

Could this thread serve to consolidate and summarize all information on L-Arg? Please help to contribute and build up this thread.

People might be interested in the following aspects about L-Arginine:

1. General uses/applications and uses with regards to PE or sexual functions.
2. Effects and actual observed results.
3. Usage - dosage, frequency, when to take, take with what else, etc.
4. Any side effects, contraindication and risk of overdosage
5. Where and what type to buy?
6. Alternatives to L-Arg
7. What else?

You go first.

Trade Name

R-Gene 10 (Pharmacia Corp.)


L-arginine is a protein amino acid present in the proteins of all life forms. It is classified as a semi-essential or conditionally essential amino acid. This means that under normal circumstances the body can synthesize sufficient L-arginine to meet physiological demands. There are, however, conditions where the body cannot. L-arginine is essential for young children and for those with certain rare genetic disorders in which synthesis of the amino acid is impaired. Some stress conditions that put an increased demand on the body for the synthesis of L-arginine include trauma (including surgical trauma), sepsis and burns. Under these conditions, L-arginine becomes essential, and it is then very important to ensure adequate dietary intake of the amino acid to meet the increased physiological demands created by these situations.

L-arginine, even when it is not an essential amino acid as defined above, is a vital one. In addition to participating in protein synthesis, it plays a number of other roles in the body. These include the detoxification of ammonia formed during the nitrogen catabolism of amino acids via the formation of urea. In addition, L-arginine is a precursor in the formation of nitric oxide, creatine, polyamines, L-glutamate, L-proline, agmatin (a possible neurotransmitter in the brain) and the arginine-containing tetrapeptide tuftsin, believed to be an immunomodulator. L-arginine is a glycogenic amino acid; it can be converted to D-glucose and glycogen if needed by the body or it can be catabolized to produce biological energy.

L-arginine, when administered in high doses, stimulates pituitary release of growth hormone and prolactin and pancreatic release of glucagon and insulin. Intravenous L-arginine may be used as an aid in the evaluation of problems with growth and stature that may be due to growth hormone deficiency. Intravenous arginine hydrochloride may be used as a fourth-line agent in the treatment of severe metabolic alkalosis. L-arginine is also used as an immunonutrient in enteral and parenteral nutrition to help improve the immune status in those suffering from sepsis, burns and trauma.

L-arginine is predominately synthesized in the kidney. It is a key intermediate in the Krebs-Henseleit urea cycle. L-ornithine and L-citrulline are precursors in the synthesis of L-arginine, and L-arginine is converted to urea and L-ornithine via the enzyme arginase. The portion of L-arginine that is not converted to urea enters the circulation, and is distributed to the various tissues and metabolized as discussed above. A much smaller amount of L-arginine is produced in the liver.

The typical dietary intake of L-arginine is 3.5 to 5 grams daily. Most dietary L-arginine comes from plant and animal proteins. Small amounts of free L-arginine are found in vegetable juices and fermented foods, such as miso and yogurt. Soy protein and other plant proteins are richer in L-arginine than are animal proteins, which are richer in lysine. It is thought that the possible hypocholesterolemic effect of soy protein is due, at least in part, to the higher L-arginine content in this protein.

L-arginine is a basic amino acid. The stereoisomer of L-arginine, D-arginine, does not have any biological activity, as far as we know. Its one-letter abbreviation is R. It is also abbreviated as Arg. The terms L-arginine and arginine are frequently used interchangeably.


Supplemental L-arginine may have anti-atherogenic, antioxidant and immunomodulatory actions. It may also have wound-repair activity.

Mechanism of Actions

Many of supplemental L-arginine’s activities, including its possible anti-atherogenic actions, may be accounted for by its role as the precursor to nitric oxide or NO. NO is produced by all tissues of the body and plays very important roles in the cardiovascular system, immune system and nervous system. NO is formed from L-arginine via the enzyme nitric oxide synthase or synthetase (NOS), and the effects of NO are mainly mediated by 3,’5’ -cyclic guanylate or cyclic GMP. NO activates the enzyme guanylate cyclase, which catalyzes the synthesis of cyclic GMP from guanosine triphosphate or GTP. Cyclic GMP is converted to guanylic acid via the enzyme cyclic GMP phosphodiesterase.

NOS is a heme-containing enzyme with some sequences similar to cytochrome P-450 reductase. Several isoforms of NOS exist, two of which are constitutive and one of which is inducible by immunological stimuli. The constitutive NOS found in the vascular endothelium is designated eNOS and that present in the brain, spinal cord and peripheral nervous system is designated nNOS. The form of NOS induced by immunological or inflammatory stimuli is known as iNOS. iNOS may be expressed constitutively in select tissues such as lung epithelium.

All the nitric oxide synthases use NADPH (reduced nicotinamide adenine dinucleotide phosphate) and oxygen (O2) as cosubstrates, as well as the cofactors FAD (flavin adenine dinucleotide), FMN (flavin mononucleotide), tetrahydrobiopterin and heme. Interestingly, ascorbic acid appears to enhance NOS activity by increasing intracellular tetrahydrobiopterin. eNOS and nNOS synthesize NO in response to an increased concentration of calcium ions or in some cases in response to calcium-independent stimuli, such as shear stress.

In vitro studies of NOS indicate that the Km of the enzyme for L-arginine is in the micromolar range. The concentration of L-arginine in endothelial cells, as well as in other cells, and in plasma is in the millimolar range. What this means is that, under physiological conditions, NOS is saturated with its L-arginine substrate. In other words, L-arginine would not be expected to be rate-limiting for the enzyme, and it would not appear that supraphysiological levels of L-arginine^which could occur with oral supplementation of the amino acid^would make any difference with regard to NO production. The reaction would appear to have reached its maximum level. However, in vivo studies have demonstrated that, under certain conditions, e.g. hypercholesterolemia, supplemental L-arginine could enhance endothelial-dependent vasodilation and NO production.

The discordance between the in vivo results^increased NO production under certain conditions^and the in vitro enzyme studies described above is known as the “arginine paradox.” There are a few explanations for the “arginine paradox.” NOS may be inhibited by asymmetric dimethylarginine or ADMA, which is known to be elevated in hypercholesterolemia and which increases mononuclear cell (monocyte and T-lymphocyte) adhesiveness in hypercholesterolemics. ADMA is formed by post-translational methylation of L-arginine residues in proteins and is released from the proteins following their hydrolysis. The “arginine paradox” may be explained in part by increasing levels of L-arginine overcoming the inhibition of NOS by ADMA. In addition to hypercholesterolemia, elevated levels of ADMA are associated with hypertension, diabetes, preeclampsia, smoking and aging. Elevation of ADMA may be due to altered metabolism of this substance by dimethylarginine dimethylaminohydrolase or DDAH. DDAH is the major enzyme involved in ADMA catabolism. Decreased levels of DDAH have been found in diabetic and hypercholesterolemic animal models.

Other explanations of the “arginine paradox” include the presence of other inhibitors of NOS yet to be discovered, impaired transport of L-arginine into or within endothelial cells and impaired regeneration of L-arginine from L-citrulline. There is another interesting possibility. A non-enzymatic pathway by which NO may be produced has recently been described. Endothelial dysfunction is associated with increased oxidative stress resulting in increased formation of such reactive oxygen species as hydrogen peroxide and superoxide anions. Further, during conditions of oxidative stress, enzymatic synthesis of NO may decrease, and NO reacts with superoxide anions to form the reactive nitrogen species peroxynitrite. Under these conditions, L-arginine can essentially scavenge hydrogen peroxide and superoxide to form NO non-enzymatically. Interestingly, in this non-enzymatic reaction, L-arginine, as well as the non-biological D-arginine, can both form NO.

NO formed from supplemental L-arginine can play a major role in the possible anti-atherogenic activity of L-arginine. NO inhibits mononuclear cell adhesion, platelet aggregation, proliferation of vascular smooth muscle, production of some reactive oxygen species, such as superoxide anions, and promotion of endothelium-dependent dilation. Leukocyte adhesion, platelet aggregation, smooth muscle proliferation, endothelial dysfunction and oxidative stress are all part of the process of atherogenesis. L-arginine may also have anti-atherogenic activity independent of its role in the enzymatic formation of NO.

L-arginine may itself have antioxidant activity. L-arginine has been found to inhibit the oxidation of low-density lipoproteins (LDL) to oxidized LDL (oxLDL). The oxidation of LDL to oxLDL is believed to be a pivotal early step in atherogenesis. L-arginine may also scavenge superoxide anions and hydrogen peroxide (see above), as well as inhibit lipid peroxidation.

L-arginine has been shown to have immunomodulatory activity. For example, in human breast cancer, supplementation with this amino acid has been reported to increase the quantity and cytotoxic activity of natural killer (NK) cells and lymphokine-activated-killer (LAK) cells. L-arginine is considered an immunonutrient and is added to enteral and parenteral feedings for burn, sepsis and trauma patients. The mechanism of L-arginine’s possible immunomodulating activity is not entirely clear. It may, at least in part, be again due to L-arginine’s role in the production of NO. Production of NO, with consequent decrease of the cyclic AMP/cyclic GMP ratio in NK cells, would favor the production of interleukin-1, which is known to activate NK cells and may directly enhance NK cell cytotoxicity. L-arginine is also a precursor in the synthesis of the tetrapeptide tuftsin, which itself appears to have immunomodulatory activity. Tuftsin’s activity appears to depend on two of the four amino acids present in its structure, L-arginine and L-proline. L-arginine also participates in the synthesis of L-proline.

L-arginine’s possible activity in wound repair may be due to its precursor role in the formation of L-ornithine and, ultimately, L-proline. L-proline is a key element in collagen biosynthesis.


Following ingestion, L-arginine is absorbed from the lumen of the small intestine into the enterocytes. Absorption is efficient and occurs by an active transport mechanism. Some metabolism of L-arginine takes place in the enterocytes. L-arginine not metabolized in the enterocytes enters the portal circulation from whence it is transported to the liver, where again some portion of the amino acid is metabolized. L-arginine not metabolized in the liver enters the systemic circulation, where it is distributed to the various tissues of the body. L-arginine participates in various metabolic activities, including the production of proteins, D-glucose, glycogen, L-ornithine, urea, nitric oxide, L-glutamate, creatine, polyamines, L-proline, agmatin and tuftsin. L-arginine is eliminated by glomerular filtration and is almost completely reabsorbed by the renal tubules. L-arginine produces peak plasma levels approximately one to two hours after oral administration.

Indications and Usage

L-arginine shows promise in the treatment and prevention of cardiovascular disease (including atherosclerosis, hypertension, hyperlipidemia and angina pectoris), in the treatment of some forms of male infertility and some kidney disorders and it is helpful in accelerating wound healing in some circumstances. It has demonstrated some positive immune-modulating and anticancer effects. There is preliminary evidence that it could be helpful in some men with erectile dysfunction and in some others with migraine, liver disease and primary ciliary dyskinesia. There is conflicting but mostly negative evidence related to claims that it can improve exercise performance and promote lean muscle mass.

Originally Posted by westla90069
You go first.

Is this sufficient?

You can refer to this url:…/lar_0024.shtml

It is too long. Will appreciate if someone can summarize it so that we can read it leisurely and at ease.

Westla, it is your turn now.

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