Nitrogen urinary excretion

The principal nitrogenous urinary excretion product in humans resulting from the catabolism of AMP is... 

The increase in diet-tissue spacing has been proposed to be caused by the effects of water and heat stress on urinary nitrogen excretion. The model has been described in detail previously (Ambrose 1991) and will be briefly summarized here Nitrogen is excreted mainly as urinary urea. Its 6 N value is substantially (2-5%o) more negative than that of the diet (Steele Daniel 1978 Yoneyama et al. 1983). Under heat and water stress the concentration... 

None of the exposures produced changes in clinical chemistry values (blood count, blood nitrate, blood urea nitrogen, serum enzymes, and serum electrolytes or urinalysis and nitrate and nitrite urinary excretion), spontaneous electrical activity of the cortex of the brain (detected by EEG), pulse rate and sinus rhythm, or pulmonary function. Visual and auditory acuity, exercise EKG, and time estimation tests did not differ from control values for any of the exposures. Only one of several cognitive tests was affected by exposure and the change occurred only in the four subjects exposed at 1.5 ppm. The test was taken during the time the subjects were experiencing severe headaches. 

Oral Treatment of hypokalemia in the following conditions With or without metabolic alkalosis digitalis intoxication familial periodic paralysis diabetic acidosis diarrhea and vomiting surgical conditions accompanied by nitrogen loss, vomiting, suction drainage, diarrhea, and increased urinary excretion of potassium certain cases of uremia hyperadrenalism starvation and debilitation corticosteroid or diuretic therapy. 

Vecuronium bromide (Norcuron) is chemically identical to pancuronium except for a tertiary amine in place of a quaternary nitrogen. However, some of the drug will exist as the bisquatemary compound, depending on body pH. Vecuronium has a moderate onset of action (2.4 minutes) and a duration of effect of about 50 minutes. Like pancuronium, it does not block ganglia or vagal neuroeffector junctions, does not release histamine, and is eliminated by urinary excretion. 

Although thiotepa is chemically less reactive than the nitrogen mustards, it is thought to act by similar mechanisms. Its oral absorption is erratic. After intravenous injection, the plasma half-life is less than 2 hours. Urinary excretion accounts for 60 to 80% of eliminated drug. 

Cll. Childs, B., Urinary excretion of free alpha-amino acid nitrogen by normal infants and children. Proc. Soc. Exptl. Biol. Med. 81, 225-226 (1952). 

Metabolic Transit of Lysinoalanine. Urinary and Fecal Excretion of Protein-Bound Lysinoalanine (113). Three different alkali-treated proteins (lactalbumin, fish protein isolate, and soya protein isolate) containing, respectively, 1.79, 0.38, and 0.14 g of lysinoalanine/16 g nitrogen were given to rats and the urines and feces were collected. Lysinoalanine was measured before and after acid hydrolysis. The fecal excretion varied from 33 to 51% of the total ingested lysinoalanine and the urinary excretion varied from 10 to 25%. The higher level of lysinoalanine found after acid hydrolysis indicates that a certain quantity is excreted in the urines as combined lysinoalanine (see Table VII). The total recovery was inferior to the ingested quantity (50 to 71%) indicating that the molecule is transformed or retained in the body of the rat. 

Faber et al. (FI) studied the effects of induced pyridoxine and pantothenic acid deficiency, obtained by use of a semisynthetic formula and deoxypyridoxine and co-methyl pantothenic acid supplements for six weeks, by determining in 5 men nitrogen retention and the urinary excretions of xanthurenic and oxalic acids during deficiency and recovery. They postulated that tissue catabolism releases suflBcient pyri-doxine to partially metabolize a tryptophan load, after which the amounts of urinary oxalic acid were sharply increased for 1-2 days. 

Hayase, K., Yokogoshi, H., and Yoshida, A. (1980). Effect of dietary proteins and amino acid deficiencies on urinary excretion of nitrogen and the urea synthesizing system in rats. /. lYirtr, no, 1327-1337. 

Other methods used to decrease the recurrence of urolithiasis include dietary modifications that decrease calcium excretion and promote diuresis. Changing the diet from alfalfa to grass or oat hay decreases the calcium intake and should decrease the urinary excretion of calcium, since fecal calcium excretion is relatively constant in horses. Although this dietary change should decrease the total calcium excretion, it may also decrease the urinary excretion of nitrogen and the daily urine volume. The latter changes could enhance the supersaturation of urine. In theory, diuresis could be promoted further by the addition of loose salt (50-75 g per day) to the concentrate portion of the diet. However, in one study where ponies were fed sodium chloride (1, 3 or 5% of the total diet dry matter (1% is approximately 75 g sodium chloride for a 500 kg horse)), there were no differences in water intake, urine production or calcium excretion. 

Prolonged bed rest is associated with increased urinary nitrogen excretion. Calcium, sodium, potassium, phosphate, and sulfate excretions are increased hydrogen ion excretion is reduced, presumably caused by decreased metabolism of skeletal muscle. The amplitude of circadian variation of plasma cortisol is reduced by prolonged immobilization, and the urinary excretion of catecholamines may be reduced to one third of the concentration in an active individual. Vanil-lylmandehc acid excretion is reduced by one fourth after 2 to 3 weeks of bed rest. 

The plasma urea nitrogen concentration decreases after birth as the infant synthesizes new protein, and the concentration does not begin to rise until tissue catabolism becomes prominent. The plasma amino acid concentration is low as a result of synthesis of tissue protein, although urinary excretion of amino acids may be quite high because of immaturity of the tubular reabsorptive mechanisms. The plasma urate concentration is high at birth, but the high clearance of urate soon reduces the plasma concentration below the adult value. 

With blindness, the normal stimulation of the hypothalamic-pituitary axis is reduced. Consequently, certain features of hypopituitarism and hypoadrenalism may be observed. In some blind individuals, the normal diurnal variation of cortisol may persist in others it does not. Urinary excretion of 17-ketosteroids and 17-hydroxycorticosteroids is reduced. Plasma sodium and chloride are often low in blind individuals, probably as a result of reduced aldosterone secretion. Plasma glucose may be reduced in blind people, and insuhn tolerance is often less. The excretion of urate is reduced. Renal function may be slightly impaired, as evidenced by slight increases in serum creatinine and urea nitrogen. 

Lesions were prominent at the corticomedullary junction where abrasion of the brush border of the tubular epithelium and desquamation of tubular epithelial cells were commonly seen. This tubular injury was associated with increased blood urea nitrogen levels and enhanced urinary excretion of endopeptidase 24.11 [156], an enzyme of the brush border of the proximal tubular epithehum. 

Using tungsten as a molybdenum antagonist, Higgins etal. (1956) demonstrated a 95-97% loss in rat intestine and liver xanthine oxidase activity, but without any notable adverse effect on the animals. However, in chicks - which use uric acid as the primary route of nitrogen excretion - oral administration of tungsten decreased urinary excretion of uric acid and caused a rise in fecal xanthine and hypoxanthine output, a reduction in growth, and an increase in mortality. 

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