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PubMed2000

Changes in free amino acid synthesis in the perfused liver of an air-breathing walking catfish, Clarias batrachus infused with ammonium chloride: a strategy to adapt under hyperammonia stress.

The changes in the free amino acid (FAA) levels, the rate of efflux of FAAs from the perfused liver, and the activity of some enzymes related to amino acid metabolism such as glutamate dehydrogenase (GDH, both reductive amination and oxidative deamination), glutamine synthetase (GS), aspartate aminotransferase (AST), and alanine aminotransferase (ALT) were studied in the liver of a freshwater air-breathing teleost, the walking catfish, Clarias batrachus, perfused with 5 and 10 mM NH(4)Cl. The level of the various non-essential FAAs increased significantly, with a total increase of about 150%, which was accompanied by a significant increase of both ammonia and urea-N in the perfused liver both with 5 and 10 mM NH(4)Cl. The rate of efflux of these non-essential FAAs from the perfused liver also increased significantly with a total increase of about 115% and 160% at 5 and 10 mM NH(4)Cl, respectively. The activity of the mentioned amino acid metabolism-related enzymes in the perfused liver also got stimulated, except for GDH in the ammonia forming direction and ALT, under a higher ammonia load. The activity (both tissue and specific) of GDH in the glutamate forming direction increased maximally, followed by AST and GS in a decreasing order. Owing to these physiological adaptive strategies related to amino acid metabolism along with the presence of a functional and regulatory urea cycle (reported earlier), it is believed that this catfish is able to survive in very high ambient ammonia or in the air or in the mud during habitat drying.

Adaptation, Physiological↗

PubMed1998

Regulation of ectodermal differentiation in Xenopus laevis animal caps treated with TPA and ammonium chloride.

Animal caps isolated from Xenopus laevis embryos at the blastula stage were treated sequentially with NH4Cl, a known cement gland inducer, and with 12-O-tetradecanoyl phorbol-13-acetate (TPA), a known neural inducer. The two artificial inducers were also used in reverse order to see if they can mimic the natural inducers acting during the progressive determination of the ectodermal organ. Immunofluorescence and whole-mount in situ hybridization were used to study the expression of tubulin, taken to indicate an early step on the pathway of cell elongation, and neural cell adhesion molecule (N-CAM) taken to indicate an early step in the determination of the nervous system. The expression of XCG-1, a marker of early specification of the cement gland, was also studied. The results showed that the two artificial inducers can mimic the effects of the natural inducers in animal cap explants. The TPA behaves like a neural inducer, reducing the number and the extension of the cement gland when added to the medium in addition to NH4Cl, before or after NH4Cl treatment. In the process of cement gland/neural induction, it is possible to redirect the ectoderm already specified as cement gland to neural tissue, but it does not seem possible to respecify the neural tissue as cement gland. Moreover, the animal caps were also cut into dorsal and ventral parts and the two halves were treated separately. The results were similar to those obtained with treatment of the entire animal cap, suggesting that a dorsal-ventral pattern is not yet established before the gastrula stage, and that in normal embryos there are boundaries between the effects of different inducers.

Ammonium Chloride↗

PubMed1985

An in vivo microperfusion study of distal tubule bicarbonate reabsorption in normal and ammonium chloride rats.

For many years it has been thought that distal nephron hydrogen ion secretion can be importantly modulated by factors such as sodium delivery, sodium avidity, and potassium stores. Free flow micropuncture studies have also indicated that the rate of bicarbonate delivery may also alter the rate of bicarbonate reabsorption. The present studies were undertaken to examine possible luminal influences on total CO2 reabsorption in microperfused distal tubules in the rat in vivo. Tubules from normal and acidotic rats were perfused with five solutions in a manner that induced changes in bicarbonate load, sodium and potassium fluxes (JNa, JK), and luminal sulfate concentration. in each collected perfusate, simultaneous analyses were undertaken to determine water reabsorption, Na, and K concentrations using graphite furnace atomic absorption spectroscopy and total CO2 by microcalorimetry. Using factorial analysis of covariance to account for confounding effects on total CO2 flux (JtCO2) such as water reabsorption, distal tubules of acidotic rats reabsorbed CO2 in the range of 50-112 pmol X min-1 X mm-1 X These JtCO2 values were not significantly correlated with HCO3 load, JNa, or JK despite changes in the latter from net reabsorption to net secretion. Distal tubules of rats with normal acid-base status had JtCO2 values which were neither significantly different from zero nor correlated with changes in JK and JNa. Further, doubling the load from 250-500 pmol/min (by doubling the perfusion rate of 25-mM HCO3 solutions) did not stimulate JtCO2 in these normal animals. Accordingly, these acute in vivo microperfusion studies indicate for the first time that neither load nor potassium or sodium fluxes are important modulators of distal tubule bicarbonate reabsorption.

Absorption↗

PubMed1986

Ammonium chloride interferes with a distinct step in the biosynthesis and cell surface expression of human melanoma-type chondroitin sulfate proteoglycan.

Human melanoma cells synthesize a cell-associated chondroitin sulfate-rich proteoglycan, whose core protein is recognized by monoclonal antibody 9.2.27. We report that the core protein is present on the surface of melanoma cells in two forms, either free or modified by the addition of chondroitin sulfate chains, suggesting that the addition of glycosaminoglycan chains may not be a prerequisite for cell surface expression of the proteoglycan core protein. Free core protein found at the cell surface does not seem to represent an overflow of the proteoglycan synthetic pathway, since experiments using a beta-D-xyloside acceptor suggest that core protein is, in fact, limiting proteoglycan synthesis. NH4Cl inhibits the synthesis of melanoma-type proteoglycan, shifting the balance of surface core protein toward the free form. The inhibition of proteoglycan synthesis is apparently not due to a disruption of enzymes and precursors involved in glycosaminoglycan synthesis, since cells treated with NH4Cl retain their ability to initiate and elongate chondroitin 4-sulfate chains on a beta-D-xyloside acceptor. In contrast, the divalent ionophore monensin inhibited core protein maturation and synthesis of glycosaminoglycan chains. The effects of both NH4Cl and monensin were reversible; thus, experiments using the drugs sequentially indicated that monensin temporally precedes NH4Cl in interfering with proteoglycan biosynthesis. Since the NH4Cl and monensin share the property of inhibiting the acidification of intracellular vesicles within cells, the present findings raise the possibility that the accessibility of proteoglycan core protein to the Golgi site of glycosaminoglycan addition is regulated in melanoma cells by acidification of intracellular compartments.

Aggrecans↗

PubMed1994

Ammonium chloride inhibits pyruvate oxidation in rat liver mitochondria: a possible cause of fatty liver in Reye's syndrome and urea cycle defects.

1. Earlier studies with liver slices showed that inhibition by NH4+ of the oxidation of palmitate to CO2 was greater than total oxidation, whereas salicylate exerted a stronger inhibitory effect on the latter. We have now investigated the effects of NH4Cl and salicylate on ADP-induced O2 consumption by mitochondria (State 3 rate) respiring on pyruvate, and oxidation of [1-14C]- and [2-14C]-pyruvate to 14CO2. 2. The rate of State 3 respiration was inhibited and plateaued at 45% with 10 mmol/l NH4Cl. 3. Oxidation of [1-14C]pyruvate was not significantly affected by either NH4Cl or salicylate. Oxidation of [2-14C]pyruvate was strongly inhibited and plateaued at 70% with 1 mmol/l NH4Cl (IC50 = 0.125 mmol/l). ADP (1 mmol/l) increased the rate of decarboxylation of [2-14C]pyruvate but the extent of NH4Cl inhibition was not affected. Salicylate had a slight activating effect in the absence or presence of NH4Cl. 4. These results indicate that NH4Cl inhibits the oxidative metabolism of acetyl-CoA in the tricarboxylic acid cycle. Therefore, inhibition of fatty acid oxidation to acetyl-CoA as well as its further oxidative metabolism occurring under hyperammonaemia (> 0.1 mmol-1.49 mmol/l in Reye's syndrome patients) may be one of the causes of fatty acidaemia. 5. The cumulative inhibitory effects of NH4+ and fatty acyl derivatives on mitochondrial oxidative metabolism and production of ATP, as well as the uncoupling effects of salicylate, may contribute to some of the pathophysiology observed in patients with Reye's syndrome, and enzyme defects of the urea cycle.

Adenosine Diphosphate↗

PubMed1990

Ammonium chloride inhibits basal degradation of newly synthesized collagen in human fetal lung fibroblasts.

The objective of this work was to characterize basal degradation of newly synthesized collagen in human fetal lung fibroblasts. Analysis of 22 separate determinations showed that in cells incubated under normal conditions, the level of intracellular degradation was normally distributed with a mean of 15.2% and a standard deviation of 2.6%. Within each experiment, however, the uncertainty (standard deviation) in determining degradation was very small, usually less than 1.5%. Consideration of the large variation between experiments and the ability of our analytic technique to detect small, but "statistically significant," differences between groups within the same experiment led us to formulate two criteria for determining whether degradation measured in cultures exposed to some agent differs in a "biologically significant" way from degradation measured in control cultures. These criteria were used to evaluate the effects of the following proteinase inhibitors on basal degradation: NH4Cl, which increases the pH of subcellular compartments that are normally acidic; and leupeptin and Na-p-tosyl-L-lysine chloromethyl ketone (TLCK), which are inhibitors of lysosomal cathepsins (B and L) that degrade collagen. NH4Cl (16 mM) lowered degradation to an extent that was both statistically and biologically significant, but neither leupeptin nor TLCK affected degradation. The effect of NH4Cl on degradation was independent of its inhibitory effects on production of collagen, protein, and ATP. These results suggest that basal degradation occurs in, or beyond, an acidic (i.e., NH4Cl-sensitive) but nonlysosomal compartment of the cell, and that NH4Cl inhibits processing within, or transport to, that compartment. This is the first report of an agent that inhibits basal degradation of newly synthesized collagen in soft tissue fibroblasts.

Adenosine Triphosphate↗

PubMed1996

Growth and fermentation responses of Selenomonas ruminantium to limiting and non-limiting concentrations of ammonium chloride.

The objective of this study was to assess fermentation product, growth rate and growth yield responses of Selenomonas ruminantium HD4 to limiting and non-limiting ammonia concentrations. The ammonia half-inhibition constant for S. ruminantium in batch culture was 296 mM. Cells were grown in continuous culture with a defined ascorbate-reduced basal medium containing either 0.5, 5, 25, 50, 100 or 200 mM NH4Cl and dilution rates were 0.07, 0.14, 0.24 or 0.40 h-1. Ammonia was the growth-limiting nutrient when 0.5 mM NH4Cl was provided and the half-saturation constant was 72 microM. Specific rates of glucose utilization and fermentation acid carbon formation were highest for 0.5 mM NH4Cl. Lactate production (moles per mole of glucose disappearing) increased at the fastest dilution rate (0.40 h-1) for 5.0 mM NH4Cl while acetate and propionate decreased when compared to slower dilutions (0.07 and 0.14 h-1). Lactate production remained low while acetate and propionate remained high for all dilution rates when NH4Cl concentrations were 25 mM or greater. Yield (Y(Glc) and Y(ATP)) were nearly doubled when NH4Cl was increased from 0.5 mM (25.1 g cells/mol glucose used and 13.9 g cells/mol ATP produced respectively) to the higher concentrations. Y(Glc) was highest at 25 mM and 50 mM NH4Cl (48.2 cells/mol and 43.1 cells/mol respectively) as was Y(ATP) (23.2 cells/mol and 20.8 cells/mol respectively). Y(NH3) was highest at the lowest NH4Cl concentration. The maximal fermentation product formation rate occurred at a growth-limiting ammonia concentration, while maximal glucose and ATP bacterial yields occurred at non-growth-limiting ammonia concentrations. Given the growth response of this ruminal bacterium, it is possible that maximization of ruminal bacterial yield may necessitate sacrificing the substrate degradation rate and vice versa.

Ammonium Chloride↗

PubMed1988

Effect of ammonium chloride on subcellular distribution of lysosomal enzymes in human fibroblasts.

Three subcellular fractions enriched in lysosomal enzyme activities have been isolated recently from human cultured fibroblasts with Percoll gradients: the dense lysosomes (DL), light lysosomes (LL), and light membranous vesicles (LM). They were shown to have different morphological, cytochemical, biochemical, and immunological properties. We now report on the dramatic but different effects of a primary amine, NH4Cl, on these subfractions. The lysosomes, as detected with a specific ultrastructural cytochemical stain for the lysosomal enzyme, arylsulfatase A, were swollen significantly in all these fractions, increasing their volumes by 64% (DL), 53% (LL), and 95% (LM), respectively. When arylsulfatase A enzyme activity was monitored, about half of the DL content was diverted to the LL. However, when newly synthesized arylsulfatase A enzyme protein was monitored with metabolic labeling and immunoprecipitation, about 80% of the enzyme protein was depleted from both the DL and LL. In contrast, neither the enzyme activity nor the newly synthesized enzyme protein of arylsulfatase A was greatly altered in the LM fraction by the treatment. Since primary amines caused newly synthesized lysosomal enzymes to diverge from the lysosomal route to a secretory pathway, it was deduced that (i) the LM fraction corresponded to a prelysosomal compartment whose lysosomal enzyme content was not affected by the amine and was thus proximal to the point of diversion between the secretory and lysosomal pathways; (ii) the LL and DL fractions were distal to the point of diversion since both fractions were depleted of their newly synthesized lysosomal enzyme; and (iii) the sorting of newly synthesized lysosomal enzyme may be different from that of the preexisting pool of the same enzyme since the LL fraction was depleted of its newly synthesized enzyme protein while accumulating excessive enzyme activity.

Ammonium Chloride↗

PubMed1989

Effects of ammonium chloride, salicylate, and carnitine on palmitic acid oxidation in rat liver slices.

To explore the possible association of hyperlipidemia with hyperammonemia and aspirin ingestion, the effects of NH4+, salicylate, and carnitine on the oxidation of [1-14C]palmitic acid to acid-soluble products (ASP) and to CO2 were investigated in rat liver slices. DL-carnitine (5 mM) increased total oxidation (ASP + CO2) more than oxidation to CO2. KCN (1.5 mM) inhibited more than 90% of the oxidation. NH4Cl inhibited the oxidation that reached a maximum at about 40 mM, but the inhibition of oxidation to CO2 (63%) was larger than that of total oxidation (30%). Carnitine did not influence NH4+ inhibition, which is consistent with the results reported for isolated mitochondria. Salicylate effects depended on salicylate concentration as well as on the presence of carnitine. In the absence of carnitine, inhibition of total oxidation reached 90% at 3 mM salicylate but that of oxidation to CO2 reached 50%. Velocity calculated at saturating palmitic acid concentration for total oxidation was slightly increased by 0.75 mM salicylate, but the increase for oxidation to CO2 was larger. At 3 mM salicylate, velocity at saturating palmitic acid concentration for the oxidation was decreased, but the decrease for oxidation to CO2 was smaller than for total oxidation. Carnitine partially relieved the inhibition of total oxidation and further increased the formation of CO2. The combination of 20 mM NH4Cl and 0.75 mM salicylate inhibited total oxidation, which was more than additive of the individual effects, and carnitine partially relieved the inhibition. It is concluded that NH4+ exerted a stronger inhibition of oxidation to CO2 than of oxidation to ASP, whereas salicylate strongly inhibited the oxidation to ASP but increased the oxidation to CO2 by uncoupling mitochondrial oxidative phosphorylation. Therefore, hyperammonemia and aspirin ingestion can inhibit fatty acid oxidation and mitochondrial metabolism that could lead to the pathophysiology seen in some childhood diseases such as Reye's syndrome. Carnitine therapy might offer some benefits.

Ammonium Chloride↗

PubMed1979

Pancreatic acinar cells: the effect of carbon dioxide, ammonium chloride and acetylcholine on intercellular communication.

1. Segments of mouse pancreatic or exorbital lacrimal gland were superfused with saline solutions. Under visual control two micro-electrodes were inserted into neighbouring cells within the same acinus or into neighbouring acini. Cell to cell electrical coupling was assessed by injecting rectangular current pulses through one electrode and measuring the electrotonic potential change in the same cell (V(1)) and in the neighbouring cell (V(2)). Acetylcholine (ACh) was added locally to impaled acini by micro-ionophoresis from an extracellular micropipette.2. Exposure of the tissues to a Krebs solution equilibrated with 100% CO(2) caused a rapid increase in the size of electrotonic potential changes in the current injection cell and disappearance of the electrotonic potential changes in a neighbouring acinus or cell. This electrical uncoupling of previously coupled cells was rapidly reversible upon return to a solution equilibrated with 95% O(2) and 5% CO(2).3. Reduction of electrical intercellular coupling was also obtained using smaller CO(2) concentrations (50, 20 or 10%). In these cases the effects developed more slowly and were less dramatic. Reducing the extracellular HCO(3) concentration enhanced the uncoupling effect of 10 or 20% CO(2). However, weak uncoupling effects were still observed using 10 or 20% CO(2) in combination with a high bicarbonate concentration maintaining a constant extracellular pH (7.4).4. Reductions in extracellular pH (down to 5.5) achieved by varying combinations of Tris base and Tris HCl had no effect on electrical coupling. Brief periods of anoxia (100% N(2)) also had no effect.5. Exposure to 20% CO(2) markedly enhanced the uncoupling effect of a brief ionophoretic pulse of ACh.6. Exposure of the tissue to 10 mM-NH(4)Cl, a procedure expected to increase the intracellular pH, counteracted the uncoupling effect of ACh. During sustained uncoupling caused by a sustained ACh stimulation a brief period of exposure to NH(4)Cl caused an immediate and fully reversible recoupling.7. It is concluded that variations in intracellular pH have marked effects on the electrical coupling between neighbouring cells in the pancreatic and lacrimal acinar tissue.

Acetylcholine↗

PubMed1993

Ammonium chloride alters renal tubular cell growth and protein turnover.

BACKGROUND: Since renal hypertrophy occurs in conditions associated with increased renal ammonia genesis it has been suggested that ammonia may stimulate renal growth. Indeed, quiescent cultured tubular epithelial cells exposed to NH4Cl undergo hypertrophy. However, ammonia inhibits liver regeneration in vivo and proliferation of cultured fibroblasts. This study was designed to evaluate the effect of ammonia (NH3/NH4+) as a regulator of kidney cell hypertrophy and also kidney cell proliferation. EXPERIMENTAL DESIGN: Cultured opossum kidney cells and primary rabbit proximal tubular epithelial cells were grown with or without (controls) NH4Cl present. RESULTS: After 3 days exposure to 5-20 mM NH4Cl, there was a dose-dependent depression of cell replication that ranged between 8 and 63% compared with controls (p < 0.017). In contrast, cell volume and protein content were significantly greater in the NH4Cl-treated cells. At 20 mM NH4Cl the protein content of treated cells exceeded that of controls by as much of 75%. This difference in protein content could, in part, be related to the disparity in cell density. However, experiments performed with cells at similar density revealed that NH4Cl also has a direct effect on cell protein content that increased by 25%; this appeared to be a consequence of depressed protein breakdown and was not due to altered protein synthesis. Experiments with rabbit kidney cells revealed that inhibition of replication was associated with a decrease in DNA [3H]thymidine incorporation. Cell cycle analysis revealed a fall in the proportion of cells in the S + G2 + M phase compared with controls (22 versus 30%, respectively; p < 0.01). NH4Cl also inhibited the burst of replication that followed chemically induced hypoxic injury of quiescent opossum kidney cells. CONCLUSIONS: We conclude that in addition to inducing hypertrophy, NH4Cl can inhibit tubular cell proliferation. Thus, while heightened ammoniagenesis in vivo may favor hypertrophy, this in vitro study raises the question whether an elevated intrarenal ammonia content might be harmful when cell replication is required. Acute tubular necrosis is a condition in which elevated ammonia levels and a requirement for cell replication coexist and could serve as an important model to study this question.

Ammonium Chloride↗

PubMed1994

Activation of acid-secreting intercalated cells in rabbit collecting duct with ammonium chloride loading.

In normal rabbit, immunolabeling of intercalated cells in the outer medullary collecting duct (OMCD) demonstrates band 3-like protein in the basolateral plasma membrane (15) and H(+)-adenosinetriphosphatase (H(+)-ATPase) in the apical plasma membrane and cytoplasmic vesicles (30). However, in type A intercalated cells in the cortical collecting duct (CCD), band 3-like protein is located primarily in multivesicular bodies and cytoplasmic vesicles (15), whereas H(+)-ATPase is present in cytoplasmic vesicles only in most intercalated cells (30). In this study, we observed the effect of chronic acid loading on immunolocalization of these transporters in the collecting duct. Adult New Zealand White rabbits received either normal tap water (controls) or 75 mM NH4Cl for 12 days plus eight daily gavages of 2-6 meq NH4Cl/kg body wt. At time of death, mean urine pH of acid-loaded animals was 5.96 (SD = 0.69), vs. 8.47 (SD = 0.07) in controls. Kidneys were fixed by in vivo perfusion and processed for light and electron microscopic immunoperoxidase localization of band 3-like protein and immunogold localization of H(+)-ATPase. In controls, band 3-like protein was largely confined to multivesicular bodies in the majority of positive-staining intercalated cells in the CCD and to the basolateral plasma membrane of intercalated cells in the OMCD. In acid-loaded rabbits, band 3 protein-positive intercalated cells in the inner CCD and the in the outer stripe of the OMCD (OMCDo) were strikingly stellate in form. Basolateral plasma membrane label was intensified, while the number of labeled multivesicular bodies was diminished. Morphometric analysis demonstrated an increase in the amount of basolateral plasma membrane in these intercalated cells. In control rabbits, H(+)-ATPase immunoreactivity in intercalated cells in the CCD was located predominantly over cytoplasmic vesicles. A minority of intercalated cells exhibited basolateral plasma membrane label, and only an occasional cell displayed apical plasma membrane label. In acid-loaded rabbits, H(+)-ATPase immunoreactivity was enhanced along the apical plasma membrane of intercalated cells in the inner CCD, and morphometric analysis demonstrated increased apical plasma membrane in band 3-positive intercalated cells in this segment. These results suggest that rabbits respond to acid loading via enhancement of both electrogenic proton secretion and Cl-/HCO3- exchange in intercalated cells in the inner CCD and the OMCDo.

Acids↗

PubMed2005

Increases in urea synthesis and the ornithine-urea cycle capacity in the giant African snail, Achatina fulica, during fasting or aestivation, or after the injection with ammonium chloride.

The objectives of this study are to determine whether a full complement of ornithine-urea cycle (OUC) enzymes is present in the hepatopancreas of the giant African snail Achatina fulica, and to investigate whether the rate of urea synthesis and the OUC capacity can be up-regulated during 23 days of fasting or aestivation, or 24 hr post-injection with NH(4)Cl (10 micromol g(-1) snail) into the foot muscle. A. fulica is ureotelic and a full complement of OUC enzymes, including carbamoyl phosphate synthetase III (CPS III), was detected from its hepatopancreas. There were significant increases in the excretion of NH(4)(+), NH(3) and urea in fasting A. fulica. Fasting had no significant effect on the tissue ammonia contents, but led to a progressive accumulation of urea, which was associated with an 18-fold increase in the rate of urea synthesis. Because fasting took place in the presence of water and because there was no change in water contents in the foot muscle and hepatopancreas, it can be concluded that the function of urea accumulation in fasting A. fulica was unrelated to water retention. Aestivation in arid conditions led to a non-progressive accumulation of urea in A. fulica. During the first 4 days and the last 3 days of the 23-day aestivation period, experimental snails exhibited significantly greater rates of urea synthesis compared with fasted snails. These increases were associated with significant increases in activities of various OUC enzymes, except CPS III, in the hepatopancreas. However, the overall urea accumulation in snails aestivated and snails fasted for 23 days were comparable. Therefore, the classical hypothesis that urea accumulation occurred to prevent water loss through evaporation during aestivation in terrestrial pulmonates may not be valid. Surprisingly, there were no accumulations of ammonia in the foot muscle and hepatopancreas of A. fulica 12 or 24 hr after NH(4)Cl was injected into the foot muscle. In contrast, the urea content in the foot muscle of A. fulica increased 4.5- and 33-fold at hour 12 and hour 24, respectively, and the respective increases in the hepatopancreas were 4.9- and 32-fold. The exogenous ammonia injected into A. fulica was apparently detoxified completely to urea. The urea synthesis rate increased 148-fold within the 24-hr experimental period, which could be the greatest increase known among animals. Simultaneously, there were significant increases in activities of glutamine synthetase (2.5-fold), CPS III (3.1-fold), ornithine transcarbamoylase (2.3-fold), argininosuccinate synthetase+lyase (13.6-fold) and arginase (3.5-fold) in the hepatopancreas 12 hr after the injection of NH(4)Cl. Taken altogether, our results support the view that the primary function of urea synthesis through the OUC in A. fulica is to defend against ammonia toxicity, but suggest that urea may have more than an excretory role in terrestrial pulmonates capable of aestivation.

Amino Acids↗

PubMed2004

Effect of ammonium chloride and dietary phosphorus in the azotaemic rat. Part II--Kidney hypertrophy and calcium deposition.

BACKGROUND: Kidney hypertrophy is stimulated by both partial nephrectomy and NH(4)Cl administration. Also, parathyroidectomy (PTX) has been reported to prevent kidney hypertrophy induced by a high protein diet. Our goal was to determine in the azotaemic rat: (i) the combined effects of NH(4)Cl administration and dietary phosphorus on the development of kidney hypertrophy and calcium deposition in the kidney and (ii) whether the absence of parathyroid hormone (PTH) affected the development of kidney hypertrophy and calcium deposition. METHODS: High (HPD, 1.2%), normal (NPD, 0.6%) or low (LPD, <0.05%) phosphorus diets were given to 5/6 nephrectomized rats for 30 days. In each dietary group, one-half of the rats were given NH(4)Cl in the drinking water. The six groups of rats were: (i) HPD + NH(4)Cl; (ii) HPD; (iii) NPD + NH(4)Cl; (iv) NPD; (v) LPD + NH(4)Cl and (vi) LPD. In a separate study, PTX was performed to determine whether PTH affected renal hypertrophy in 5/6 nephrectomized rats given NH(4)Cl. RESULTS: Both with and without NH(4)Cl (+/-NH(4)Cl), kidney weight was greatest (P<0.05) in the HPD groups. In each dietary phosphorus group, kidney weight was greater (P<0.05) in the NH(4)Cl group. In both the +/-NH(4)Cl groups, kidney calcium content was greatest (P<0.05) in the HPD group, but was less (P<0.05) in the NPD and HPD groups given NH(4)Cl. An inverse correlation was present between creatinine clearance and kidney calcium content (r = -0.51, P<0.001). When factored for kidney weight, creatinine clearance was less (P<0.05) in the HPD group in both the +/-NH(4)Cl groups, but was greater in the HPD + NH(4)Cl than in the HPD group. In PTX rats, kidney weight was greater (P<0.05) and kidney calcium deposition was less (P<0.05) in rats given NH(4)Cl. CONCLUSIONS: In azotaemic rats studied for 30 days, NH(4)Cl administration induced kidney hypertrophy. A HPD also induced kidney hypertrophy. The effects on kidney calcium deposition were divergent for which NH(4)Cl administration decreased and a HPD increased calcium deposition. The inverse correlation between kidney calcium content and creatinine clearance suggests that kidney calcium deposition is harmful to renal function. When factored for kidney weight, the lower creatinine clearance in the high phosphorus group suggests that kidney hypertrophy does not completely compensate for the harmful effects of a HPD. This result also suggests that a longer study would probably result in more rapid deterioration in the high phosphorus group. In PTX rats, the absence of PTH did not prevent NH(4)Cl from inducing kidney hypertrophy and reducing kidney calcium deposition. In conclusion, NH(4)Cl and dietary phosphorus each independently affect kidney growth and calcium deposition in the growing rat with renal failure.

Ammonium Chloride↗

PubMed1967