Plasma arginine

Neuroendocrine Tobacco smoking is acutely related to elevations in plasma arginine vasopressin, neurophs I, j8-endorphin, and j8-lipotropin (Pomerleau et al. 1983). Cigarette smoking elevates plasma cortisol levels via a central mechanism in the hypothalamus or brain stem... 

Consideration of other plasma amino acids also informs the diagnosis of inborn errors of urea synthesis. The plasma concentrations of glutamine and alanine are often elevated in parallel with or prior to the ammonium concentration as they act as a nitrogen buffer. Plasma arginine concentrations are low since the only synthetic route for arginine in humans is via the urea cycle. In contrast, the arginine concentration is elevated in ARG-1 deficiency. Hyperornithinemia and homocitrullinuria are the characteristic features of the hyperammonemia, hyperornithinemia, and homocitrullinuria (HHH) syndrome caused by a defect in the ornithine transporter (ORNT-1). 

Particular interest attaches to these amino acids which are intermediary metabolites of the urea cycle, and which are normally present in the plasma, ornithine, citrulline, and arginine. Earlier reports do not mention the levels of these amino acids. Moser et al. (M13) found a normal plasma ornithine level in their two patients, but the citrulline was, as would be expected, several times the normal level, while the plasma arginine was at the lower limit of normal. In the cerebrospinal fluid also the citrulline level was greatly increased, while the ornithine and arginine levels were normal. Similar results were obtained also by Carton et al. (C3) in their neonate who died at 6 days old, and by Levin et al. (L5, Lll), also in a neonate who died in the first week of life. In the last two cases, however, the levels of citrulline were considerably higher than in the older patient of Moser et al. (M13) at 2.2 mg and 3.0 mg/100 ml, compared with a level of only 0.77 mg/100 ml for Moser s... 

The changes in levels of amino acids other than glutamine in the cerebrospinal fluid in hyperammonemia are variable. In two reported instances (L3, L6), the arginine level was low, 30-50% of the normal. This could be a reflection of the decreased plasma arginine level or possibly of the block in the urea cycle in the brain itself. On the other hand, in another instance (LIO), the arginine level was normal. The changes in the other amino acids are also not consistent. In any case, the cerebrospinal fluid levels of amino acids are so low that such changes as were found are difiicult to interpret with certainty (Table 6). 

The mass spectrum shows an abundant molecular ion and the derivatization procedure is a simple one-step reaction with trifluoroacetic anhydride/trifluoroacetic acid (1 1). The 2-perfluoroalkyl-3-oxazolin-5-one (FOx) derivatives appear to have significant potential for the low level definitive determination of difficult amino acids and labelled amino acids, as seen in the recent application to plasma arginine [175]. 

The inherited enzyme deficiencies listed in Table 11.2 lead to the accumulation of substrates and deficiencies of products. For correct interpretation of laboratory results, one need be aware that substrate accumulation can affect the prior enzyme in the pathway (e.g. increased carbamyl phosphate inhibits CPS). A deficiency of urea cycle intermediates (transport or enzyme products or dietary substances) e.g. arginine or ornithine, is often rate limiting. It can initiate a vicious cycle, which worsens the urea synthetic capacity in the cytosol (e.g. by limiting protein synthesis), or in the mitochondria (deficient stimulation of NAGS and of substrate for OTC). Measured plasma values reflect cytosolic metabolite concentrations, not those of mitochondria. Protein catabolism contributes to the plasma amino acid values. Thus, the interpretation of results for plasma arginine, proline and lysine must be done within the context of the pattern found for all of the amino acids. Urea concentrations depend upon the arginine in the cytosol originating from protein catabolism, urea cycle synthesis, and therapeutic applications. 

Castillo, L., T.E. Ch man, M. Sanehez, Y. M. Yu, J. F. Burke, A.M. Ajami, J. Vogt, and V.R. Young, 1993. Plasma arginine and eitrulline kineties in adults given adequate and arginine-free diets. Proc. Natl. Acad. Sci. USA 90, 7749-7753. 

Change of plasma arginine flux around weaning period in young calves... 

Table 1. Feed intake and plasma arginine flux determined by intravenous infusion or oral administration arginine in pre- (2 and 6 weeks) and post-weaning (10 weeks) calves. 

Logically, ADH receptor antagonists, and ADH synthesis and release inhibitors can be effective aquaretics. ADH, 8-arginine vasopressin [113-79-17, is synthesized in the hypothalamus of the brain, and is transported through the supraopticohypophyseal tract to the posterior pituitary where it is stored. Upon sensing an increase of plasma osmolaUty by brain osmoreceptors or a decrease of blood volume or blood pressure detected by the baroreceptors and volume receptors, ADH is released into the blood circulation it activates vasopressin receptors in blood vessels to raise blood pressure, and vasopressin V2 receptors of the nephrons of the kidney to retain water and electrolytes to expand the blood volume. 

Hyperargininemia. This defect is characterized by elevated blood and cerebrospinal fluid arginine levels, low erythrocyte levels of arginase (reaction 5, Figure 29-9), and a urinary amino acid pattern resembling that of lysine-cystinuria. This pattern may reflect competition by arginine with lysine and cystine for reabsorption in the renal tubule. A low-protein diet lowers plasma ammonia levels and abolishes lysine-cystinuria. 

Primary therapy is based on disease severity and type of hemorrhage.7 Most patients with mild to moderate disease and a minor bleeding episode can be treated with l-desamino-8-D-arginine vasopressin [desmopressin acetate (DDAVP)], a synthetic analog of the antidiuretic hormone vasopressin. DDAVP causes release of von Willebrand factor (vWF) and factor VIII from endogenous storage sites. This formulation increases plasma factor VIII levels by three- to fivefold within 30 minutes. The recommended dose is 0.3 mcg/kg intravenously (in 50 mL normal saline infused over 15 to 30 minutes) or subcutaneously or 300 meg intranasally via concentrated nasal spray every 12 hours. Peak effect with intranasal administration occurs 60 to 90 minutes after administration, which is somewhat later than with intravenous administration. Desmopressin infusion may be administered daily for up to 2 to 3 days. Tachyphylaxis, an attenuated response with repeated administration, may occur after several doses.8... 

ROS can modify amino acid side chains, with histidine, tryptophan, cysteine, proline, arginine, and lysine among those most susceptible to attack (Brown and Kelly 1994). As a result, carbonyl groups are generated, and these carbonyl concentrations can be measured directly in plasma by using atomic absorption spectroscopy, fluorescence spectroscopy, or HPLC following reaction with 2,4-dinitrophenylhydrazine. 

A comprehensive, randomized, placebo-controlled trial of infused bolus L-arg and its enantiomer (D-arg) included healthy subjects, non-insulin dependent diabetics, hypertensive subjects, and normotensives with primary hypercholesterolemia [147]. A blood-pressure drop and an acute inhibition of ADP-induced aggregation in platelet-rich plasma were observed in all subjects after L-arg administration (<5 g). Both responses to L-arg infusion closely correlated in magnitude, were weaker in noninsulin dependent diabetics and hypercholesterolemics, and declined with increasing age. Notably, D-arg did not elicit any of the L-arg effects, which were reduced by some 70% when superimposed upon ongoing, nonselective NOS inhibition with infused L-N-monomethyl-arginine (L-NMMA). Since D-arg is not a NOS substrate, and L-NMMA is a substrate-competitive NOS inhibitor, the L-arg effects observed in this study were theorized to reflect a rise in vascular NO production by eNOS. In contrast, the inhibition of platelet aggregation observed in vitro after a 5 min L-arg infusion (160 mg total dose) into healthy subjects and patients with angiographic... 

The above experiments strongly suggest to us that a linear relationship exists between serum or plasma insulin levels over a wide physiological range, and urinary calcium excretion. The calciuric response to arginine or glucose infusion does not occur if insulin secretion is prevented, as evidenced by the data obtained from animals made acutely insulinopenic by mannoheptulose, or more chronically diabetic by streptozotocin. 

The standard diet used in our experiments is a semipurified, cholesterol-free preparation that is composed of 25% protein, 40% sucrose, 13% coconut oil, 1% corn oil, 15% cellulose, 5% mineral mix, and 1% vitamin mix. This diet has been shown to induce an endogenous hypercholesterolemia and lead to atherosclerosis in rabbits and monkeys (4, 5). The specific question addressed by our series of investigations is whether the type of dietary protein, when all other dietary components are constant, can influence the development of hyperlipoproteinemia and atherosclerosis. More specifically, we have examined the effects of the individual amino acids, lysine and arginine, and their ratios in the diet on plasma and hepatic lipids as well as the development of arterial plaques. 

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