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l-Arginine, the substrate for NO synthesis: An alternative …
This is a semi-essential amino acid, because although it is normally synthesized in sufficient amounts by the body, supplementation is sometimes required (for example, due to inborn errors of urea synthesis, protein malnutrition, excessive lysine intake, burns, peritoneal dialysis, and rapid growth).
An alternative explanation for the effect of iNOS induction on eNOS function is provided by the observation that addition of -arginine induced formation of NO in the artery wall (and relaxation), showing that endogenous -arginine is insufficient to feed the available pool of iNOS. Previous work has shown that when NOS (including iNOS) is starved of saturating concentrations of -arginine, the enzyme can produce superoxide anion (). Thus, we may postulate that the iNOS, induced by endotoxin incubation, generates significant levels of superoxide in the artery wall, and this superoxide excess is then able to degrade NO chemically. An observation that is consistent with this hypothesis is the finding that overexpression of eNOS protected against the fall in blood pressure and lung injury caused by endotoxin (). In the latter study, the additional eNOS may be forming enhanced levels of NO that can overcome the superoxide formed from iNOS.
Extracellular L-arginine is required for optimal NO synthesis …
In addition to the impairment of carbachol-induced eNOS activation, the present experiments provide evidence for changes in the action of NO (either generated by carbachol and measured with the microsensor or supplied by the NO donor spermine NONOate). Thus, -arginine administration (present 20 min before carbachol) restored NO output to control levels but relaxation was still impaired, suggesting a dysfunction of the NO-signalling pathway. However, when -arginine was present during both the incubation and test periods, the NO output induced a greater relaxation than when the -arginine was added 20 min before carbachol, from which it can be concluded that impairment of NO signalling occurred during the long period of endotoxin administration. This was confirmed by the addition of -arginine during incubation with endotoxin (but absent during the carbachol test), which also reduced the effect of endotoxin on NO action, but did not change NO formation. It is possible that -arginine, which is known to have antioxidant action, may in part produce this effect by protecting against detrimental consequences of superoxide anion generation. Thus, our results suggest a close parallelism between NO synthesis and NO action in the artery wall, both of which were reduced as a result of superoxide formation (not as a result of excess NO formation) from iNOS. However, there is a difference in the time course since inhibition of NO action built up during the 4 h incubation with endotoxin, whereas the inhibition of eNOS could be rapidly reversed.
Several studies have hypothesised that the interaction between iNOS and eNOS depends on excessive formation of NO by iNOS, which then either downregulates or inactivates eNOS (; ). However, in the present study, it was found that addition of -arginine, 20 min before carbachol, was able to restore NO concentration to normal. This result argues against an impairment developing during the long exposure to endotoxin, as would be required for downregulation of eNOS protein synthesis. It also suggests that the endotoxin-mediated impairment of arterial function is not due to excess NO.
All about protein: What is it and how much do you need?
The augmentation of carbachol's action by 100 μ-arginine was blocked by two inhibitors of the cationic amino-acid transporter (-lysine and gramicidin) and by incubation with a caveolin antibody. Thus, it is likely that the additional NO formed when -arginine is administered to the Krebs' solution, requires uptake of -arginine into endothelial cells using the cationic amino-acid transporter. There is evidence that some eNOS is located within caveolae, possibly isolating it from the large internal store of -arginine (). Caveolins are specific membrane proteins located in caveolae that may regulate eNOS () and may link it to the cationic amino-acid transporter. The effect of anticaveolin in the present experiments suggests that some functional eNOS is located at the caveoli. Anticaveolin may act by uncoupling caveolin from the cationic amino-acid transporter, or may prevent access of -arginine to the transporter site or may perhaps prevent a necessary conformational change in caveolin/transporter complex. In the absence of extracellular -arginine, none of the interventions (-lysine, gramicidin or anti-caveolin) had any effect on carbachol-induced relaxation, suggesting that adequate NO output can be maintained without reuptake or transmembrane cycling of endogenous -arginine.
Addition of 100 μ-arginine to the Krebs' solution 20 min before carbachol (but absent during endotoxin administration), restored carbachol-induced NO to normal (). Carbachol-induced relaxation, although enhanced by -arginine, was not restored to control level (). In contrast, addition of -arginine during incubation with endotoxin (but absent during carbachol administration) did not restore NO formation. However, there was some restoration of relaxation in response to carbachol, but relaxation was not restored to control levels (). These experiments show that -arginine administration can protect eNOS against damage resulting from induction of iNOS, and that the critical time is during activation of eNOS by carbachol.
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L-arginine is an amino acid necessary for protein synthesis
Spontaneous, nonenzymatic breakdown of creatine and creatine phosphate to creatinine causes the excretion of 1 to 2 g creatinine/d and requires the replacement of an equivalent amount of creatine from the diet and by endogenous synthesis.
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Renal arginine synthesis in humans produces approximately 2 g /d, which may be compared to an intake, from a Western diet, of approximately 4 to 5 g/d.
Arginine Alpha-Ketoglutarate - latest research | …
Arjmandi found that when six grams of the amino acid L-citrulline / L-arginine from watermelon extract was administered daily for six weeks, there was improved arterial function and consequently lowered aortic blood pressure in all nine of their prehypertensive subjects (four men and five postmenopausal women, ages 51-57).
Response: It would help to see additional studies to determine whether the results are consistent and what the required dosage would be.
03/10/2017 · Muscle Growth
The first enzyme of creatine biosynthesis, L-arginine:glycine amidinotransferase, occurs in the kidney and produces guanidinoacetate, which is released into the renal vein.
L-arginine Benefits Heart Health & Performance - Dr. Axe
Aging is associated with anabolic resistance, a reduced sensitivity of myofibrillar protein synthesis (MPS) to postprandial hyperaminoacidemia, particularly with low protein doses.
Liquid L-Arginine-Reduce Artery Plaque-Unclog Arteries
L It is a semi-essential amino acid synthesized by the body from ornithine. This amino acid supports protein synthesis as it is involved in the transport and storage of nitrogen. Among many functions, it is used by the body to produce creatine.
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