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PubMed1995

Lung function and chronic respiratory symptoms of pig farmers: focus on exposure to endotoxins and ammonia and use of disinfectants.

OBJECTIVES: The prevalence of chronic respiratory symptoms among pig farmers is known to be high, but the aetiology of these symptoms is not yet unravelled. Long term average exposure to dust was evaluated, endotoxins and ammonia and use of disinfectants were compared with chronic respiratory symptoms and depressed base line lung function. METHODS: A cross sectional study was performed among 194 Dutch pig farmers, of whom 100 had not and 94 had chronic respiratory symptoms. Exposure-response relations were evaluated with multiple logistic and linear regression analysis. Estimates of long term average exposure were based on two personal exposure measurements, taken on one day in summer and one day in winter. Information on use of disinfectants and disinfection procedures was assessed by a walk through survey and interview by telephone. RESULTS: Exposure to dust, endotoxins, and ammonia were not related to chronic respiratory symptoms. Duration of the disinfection procedure and pressure used at disinfection were strongly and positively related to chronic respiratory symptoms. A significant inverse association between base line lung function and endotoxin exposure was found only among asymptomatic farmers. Ammonia exposure and duration of the disinfection procedure were significantly associated with base line lung function in the entire population. CONCLUSION: Results suggest that use of disinfectants is an important aetiological factor in chronic respiratory health effects of pig farmers. This factor has not been studied before. Results also suggest an aetiological role for exposure to endotoxins and ammonia in development of chronic respiratory health effects, but longitudinal studies with detailed exposure assessment strategies are required to assess their roles.

Adult↗
PubMed1981

Cell-free ammonia-oxidizing system of Nitrosomonas europaea: general conditions and properties.

Conditions essential for the preparation of active ammonia-oxidizing extracts of Nitrosomonas europaea were studied. The extracts were unstable during storage and required specific assay conditions for ammonia oxidation. Bovine serum albumin, spermine, or MgCl2 was required for ammonia oxidation and the concentration of phosphate determined the relative effectiveness of each activator, i.e., albumin being most effective in 0.1 M phosphate and spermine or MgCl2 at lower phosphate concentrations. Kinetic experiments showed a partial reduction of cytochrome c preceding the initiation of oxygen consumption due to ammonia oxidation.

Ammonia↗
PubMed1982

Distribution of 13N following intravenous injection of [13N]ammonia in the rat.

Ammonia labeled with cyclotron-produced 13N was injected intravenously in rats and the content of 13N in 14 major organs and tissues was determined at eight intervals ranging from 0.2 to 50 min after injection. The distribution of 13N at 12 s was employed to estimate the unidirectional tissue extraction for ammonia. The estimated fractional extraction for most of the tissues studied ranged from 70 to 100%. The 12-s 13N concentrations in a number of tissues (with lungs and brain the principal exceptions) were found to be quite similar to those reported for 42K+ and 86Rb+ in the rat, suggesting a similar mechanism to transcapillary extraction. Most of the injected dose was initially extracted by the musculature, lungs, and kidneys. The lungs and kidneys released the bulk of their extracted ammonia-derived nitrogen within 10 min of injection. The gut, heart, and spleen also recirculated extracted nitrogen, but on a much smaller scale than the lungs and kidneys. The recirculated label was accumulated mainly by muscle, liver, and skin. The results suggest that the lungs and kidneys are important sources of systemically recirculated ammonia metabolites in the rat.

Ammonia↗
PubMed1978

Plasma ammonia and liver ornithine transcarbamoylase activity in zinc-deficient rats.

The effects of zinc deficiency on the activity of hepatic ornithine carbamoyltransferase (OCT) and plasma ammonia were studied in rats. One group received (ad libitum) zinc-deficient diet containing 2 ppm zinc and the other group received a diet containing 110 ppm zinc (group pair-fed control) equal to the amount consumed by zinc-deficient rats during the previous 24 h. Rats were killed at weekly intervals. Blood urea nitrogen (BUN), plasma ammonia, and hepatic OCT activity were determined. By end of the 1st wk on zinc-deficient diet, the plasma ammonia levels became significantly higher than those of the controls and remained elevated thoughout the study period. BUN increased initially for 2 wk in the deficient rats, but by the end of 4 wk the levels were lower than in the controls. The hepatic OCT activity in deficient animals was significantly lowered as compared to the controls by the 3rd wk. It is concluded that an increase in plasma ammonia may occur as a result of deficiency of zinc.

Ammonia↗
PubMed2000

Luminal ammonia retards restitution of guinea pig injured gastric mucosa in vitro.

The present study was conducted to elucidate the mechanisms by which Helicobacter pylori (HP)-derived ammonia causes gastric mucosal injury. Intact sheets of guinea pig gastric fundic mucosae were incubated in Ussing chambers. Both the luminal and the serosal pH were kept at 7.4. Transmucosal potential difference (PD) and electrical resistance (R) were monitored as indices of mucosal integrity. Restitution was evaluated by recovery of PD, R, and transmucosal [(3)H]mannitol flux after Triton X-100-induced mucosal injury. The effects of luminal or serosal NH(4)Cl on function and morphology of uninjured or injured mucosae were examined. In uninjured mucosae, serosal NH(4)Cl induced more profound decreases in PD and R and more prominent vacuolation in gastric epithelial cells than did luminal NH(4)Cl. In contrast, luminal NH(4)Cl markedly inhibited restitution in injured mucosae and caused an extensive vacuolation in gastric epithelial cells, as did serosal NH(4)Cl. Transmucosal ammonia flux was greater in the injured than in the uninjured mucosae. These results suggest that 1) basolateral membrane of gastric epithelial cells is more permeable to ammonia than apical membrane and 2) luminal ammonia, at concentrations detected in HP-infected gastric lumen, retards restitution in injured mucosae.

Ammonia↗
PubMed1990

Diaphragm does not produce ammonia or lactate during high-intensity short-term exercise.

To ascertain whether costal diaphragm engages in ammonia and lactate production (like limb muscles) during high-intensity short-term exercise, experiments were carried out on six healthy trained ponies in which phrenic venous catheters had been implanted 5-9 days earlier. Simultaneous anaerobically obtained blood samples from abdominal aorta and the phrenic vein at rest and during 4 min of exertion at 32 km/h and at a 7% grade were analyzed for blood-gas variables as well as lactate and ammonia concentrations using standard procedures. At rest, heart rate was 47 +/- 4 beats/min and the diaphragmatic O2 extraction was 26.5%. With exercise, heart rate rose to 218 +/- 6 beats/min, marked acidosis and hyperventilation occurred, and the diaphragmatic O2 extraction increased threefold (80.9%). Such exercise is known to dramatically increase the work of breathing as respiratory frequency and change in pleural pressure approach 138 +/- 4 breaths/min and 30 +/- 3 cmH2O, respectively. Despite the fact that phrenic-venous O2 tension of exercised ponies decreased to 15.5 +/- 0.6 Torr, the phrenic-venous lactate and ammonia concentrations did not exceed corresponding arterial values. These data thus revealed that the diaphragm is uniquely unlike limb muscles, which at high workloads readily engage in net ammonia and lactate production, and that the diaphragmatic energy needs during high-intensity short-term exercise are primarily met by aerobic metabolism.

Ammonia↗
PubMed1975

Potassium-sparing effect of enhanced renal ammonia production.

The effect of a primary alteration in renal ammonia production on potassium excretion was explored in normal men utilizing ingestion of glutamine to increase ammonia production independent of concomitant acid-base manipulations. After ingesting a constant-formula diet of normal electrolyte content for 3 days, normal men underwent on separate occasions in a rigidly paired fashion an acute study with ingestion of glutamine (4.3 mmol/kg) or only water. Glutamine ingestion under conditions of normal acidification or concomitant with an acute acidifying stimulus resulted in an increase in ammonium and concomitant decrease in potassium excretion. The potassium conservation could not be accounted for by changes in urinary sodium excretion or in plasma potassium or acid-base parameters. Furthermore, when NaHCO3 was ingested for 3 days preceding both the water and glutamine studies, the influence of glutamine on both ammonium and potassium excretion was reduced significantly. These studies suggest that altered ammonia production can affect potassium excretion, providing further evidence in support of a renal potassium-ammonia homeostatic mechanism.

Acid-Base Equilibrium↗
PubMed2005

Characterization of ammonia transport by the kidney Rh glycoproteins RhBG and RhCG.

The erythrocyte Rh-associated glycoprotein (RhAG) was recently found to mediate transport of ammonia/ammonium when expressed in Xenopus laevis oocytes and yeast Saccharomyces cerevisiae. Nonerythroid homologs, RhBG and RhCG, are expressed in the mammalian kidney connecting segment and the collecting duct, major sites of urinary ammonia secretion. This study characterizes the transport properties of murine RhBG and RhCG by ammonium analog [14C]methylamine (MA) uptake and two-electrode voltage clamping of X. laevis oocytes. Both RhBG and RhCG mediated transport of ammonia, but differed in affinity for substrate (K(m) = 2.5 and 10 mM, respectively). The rates of RhBG- and RhCG-mediated transport were sensitive to the concentration of the protonated MA species and were stimulated by extracellular alkalosis and inhibited by acidosis, suggesting a role for H+ in the transport process. Whereas expression of RhBG or RhCG caused a small increase in plasma membrane conductance, [14C]MA uptake was not affected by depolarization of oocytes with 100 mM extracellular K+ or by clamping the membrane potential between 0 and -100 mV, indicating that RhBG- and RhCG-mediated transport was independent of the membrane potential. These results strongly suggest that RhBG and RhCG transport ammonia by an electroneutral process that involves NH4(+)/H+ exchange resulting in net NH3 translocation. The polarized localization of RhBG and RhCG in kidney tubules and the different substrate affinities may enable these proteins to participate in transepithelial ammonia secretion and to therefore play an important role in whole animal acid-base regulation.

Ammonia↗
PubMed2005

Renal expression of the ammonia transporters, Rhbg and Rhcg, in response to chronic metabolic acidosis.

Chronic metabolic acidosis induces dramatic increases in net acid excretion that are predominantly due to increases in urinary ammonia excretion. The current study examines whether this increase is associated with changes in the expression of the renal ammonia transporter family members, Rh B glycoprotein (Rhbg) and Rh C glycoprotein (Rhcg). Chronic metabolic acidosis was induced in Sprague-Dawley rats by HCl ingestion for 1 wk; control animals were pair-fed. After 1 wk, metabolic acidosis had developed, and urinary ammonia excretion increased significantly. Rhcg protein expression was increased in both the outer medulla and the base of the inner medulla. Intercalated cells in the outer medullary collecting duct (OMCD) and in the inner medullary collecting duct (IMCD) in acid-loaded animals protruded into the tubule lumen and had a sharp, discrete band of apical Rhcg immunoreactivity, compared with a flatter cell profile and a broad band of apical immunolabel in control kidneys. In addition, basolateral Rhcg immunoreactivity was observed in both control and acidotic kidneys. Cortical Rhcg protein expression and immunoreactivity were not detectably altered. Rhcg mRNA expression was not significantly altered in the cortex, outer medulla, or inner medulla by chronic metabolic acidosis. Rhbg protein and mRNA expression were unchanged in the cortex, outer and inner medulla, and no changes in Rhbg immunolabel were evident in these regions. We conclude that chronic metabolic acidosis increases Rhcg protein expression in intercalated cells in the OMCD and in the IMCD, where it is likely to mediate an important role in the increased urinary ammonia excretion.

Acidosis, Renal Tubular↗
PubMed2000

Effects of ammonia on bicarbonate transport in the cortical collecting duct.

Both acidosis and hypokalemia stimulate renal ammoniagenesis, and both regulate urinary proton and potassium excretion. We hypothesized that ammonia might play an important role in this processing by stimulating H(+)-K(+)-ATPase-mediated ion transport. Rabbit cortical collecting ducts (CCD) were studied using in vitro microperfusion, bicarbonate reabsorption was measured using microcalorimetry, and intracellular pH (pH(i)) was measured using the fluorescent, pH-sensitive dye, 2', 7'-bis(2-carboxyethyl)-5(6)-carboxyfluorescein (BCECF). Ammonia caused a concentration-dependent increase in net bicarbonate reabsorption that was inhibited by luminal addition of either of the H(+)-K(+)-ATPase inhibitors, Sch-28080 or ouabain. The stimulation of net bicarbonate reabsorption was not mediated through apical H(+)-ATPase, basolateral Na(+)-K(+)-ATPase, or luminal electronegativity. Although ammonia caused intracellular acidification, similar changes in pH(i) induced by inhibiting basolateral Na(+)/H(+) exchange did not alter net bicarbonate reabsorption. We conclude that ammonia regulates CCD proton and potassium transport, at least in part, by stimulating apical H(+)-K(+)-ATPase.

Ammonia↗
PubMed1984

Silicone rubber membrane for extraction of high vapor tension toxic substances. Experiences with ammonia and ethanol.

The purpose of this study is to evaluate the permeability of a silicone rubber membrane to two toxic substances, ammonia and ethanol, under high vapor tension. A device was assembled for testing the diffusion of the substances through a silicone rubber membrane interposed between two aqueous phases. 9 experiences were carried out with ammonia at different temperatures: 3 at 11 degrees C, 3 at 24 degrees C and 3 at 37 degrees C. 8 experiences were carried out with ethanol at different temperatures: 3 at 11 degrees C, 3 at 24 degrees C and 2 at 37 degrees C. Mean transmembrane flow (mumol/m2 X h) for ammonia was 43.99 at 11 degrees C, 59.18 at 24 degrees C and 145.45 at 37 degrees C. Mean transmembrane flow (mmol/m2 X h) for ethanol was 6.48 at 11 degrees C, 12.54 at 24 degrees C and 22.51 at 37 degrees C. The results confirm that ammonia and ethanol in water solution can pass through a silicone rubber membrane. Better results could be expected with both aqueous phases in motion as in dialysis devices.

Ammonia↗
PubMedDate not supplied

Gastric mucosal damage and adaptive protection by ammonia and ammonium ion in rats.

Helicobacter pylori (Hp) is considered as the major pathogen in Hp-associated gastritis but the mechanism of its action has not been fully explained. We investigated both the damaging and protective effects of intragastric (i.g.) application of ammonia (NH4OH) and ammonium ion (NH4Cl), the major products of Hp-derived urease, on the rat stomach with intact and capsaicin-deactivated sensory nerves or suppressed prostaglandin (PG) and nitric oxide (NO) synthesis. NH4OH given i.g. resulted in a concentration-dependent mucosal damage starting at 30 mM and reaching maximum at 250 mM (pH 11), the extent of damage being similar to that obtained with 100% ethanol. NaOH solution (1 mM) at pH 11 given i.g. did not affect mucosal integrity. The damage caused by NH4OH was accompanied by the fall in gastric blood flow (GBF) reaching at 250 mM NH4OH about 30% of the vehicle control value. The NH4OH-induced gastric damage was augmented by capsaicin-induced deactivation of sensory nerves, the suppression of nitric oxide (NO) synthase with L-NAME or the decrease of i.g. acidity by ranitidine. The pretreatment with scavengers of reactive oxidants significantly reduced the area of NH4OH-induced gastric lesions. When the mucosa was first exposed to a low 15-mM concentration of NH4OH and then insulted with large 250 mM NH4OH or with 100% ethanol, the lesion area was markedly reduced as compared to that obtained with 250 mM NH4OH or 100% ethanol alone. This adaptive protection by 'mild' concentration of NH4OH against strong irritants (250 mM NH4OH or 100% ethanol) was reversed, in part, by pretreatment with L-NAME and indomethacin. NH4Cl (60-500 mM) given i.g. alone failed to affect the mucosal integrity but when applied before 100% ethanol it produced a concentration-dependent fall in the mucosal damage by these irritants. We conclude that; (1) ammonia at higher concentrations damages the gastric mucosa, while ammonium ion exerts the protective activity; (2) the ammonia-induced gastric damage may involve the formation of reactive oxidants; (3) ammonia at lower concentration acts like a mild irritant via the activation of sensory nerves, NO-arginine pathway and PG.

Adaptation, Physiological↗
PubMed1997

In vitro ammonia utilization and urea synthesis by rat liver after portacaval shunt.

BACKGROUND: The objective of this study was to study in vitro ammonia utilization and urea synthesis by the rat liver after portacaval shunt (PCS) in comparison to controls. This study is part of a series of experiments to investigate metabolic derangements in the liver following PCS. METHODS: Sixteen male Wistar rats weighing 150-230 g were used. PCS was performed on 8 and the rest served as sham-operated controls. The experiments were performed 4 weeks postoperatively. The usually monitored postoperative parameters after PCS like body weight, rise in ammonia levels in the peripheral blood, atrophy of mesenteric fat, atrophy of the liver, etc., were comparable to other PCS series. Liver slices (1 x 2 x 1 mm) were prepared from each rat liver and incubated in Krebs-Henseleit buffer. RESULTS: After incubation, ammonia utilization in the controls was 162.88+/-20.12 micromol/g dry weight/h while in PCS rats it was 81.35+/-2.64 micromol/g dry weight/h (p < 0.0001). The rate of urea synthesis in controls was 122.54+/-12.93 micromol/g dry weight/h whereas in the PCS group it was 14.99+/-2.21 micromol/g dry weight/h (p < 0.0001). CONCLUSION: These results indicate a significant decline in the capacity of the liver for ammonia utilization as well as urea synthesis after PCS.

Ammonia↗
PubMed1992

Quantification of regional myocardial blood flow using 13N-ammonia and reoriented dynamic positron emission tomographic imaging.

BACKGROUND: Regional myocardial blood flow has been quantified using transaxial positron emission tomographic (PET) imaging and tracer kinetic modeling. However, the use of transaxial images limits the accuracy of regional partial volume corrections and the localization of the quantified regional flow values. The purpose of the present study was to overcome both problems by calculating regional flows from reoriented short-axis PET images. METHODS AND RESULTS: Twelve experiments were performed in four dogs. 13N-ammonia was injected intravenously while microspheres were administered into the left atrium during baseline, hyperemic, and low-flow conditions. Serial transaxial frames were acquired with a 15-plane PET scanner and reoriented into short-axis frames. The arterial input function and eight regional myocardial tissue activity curves were derived from the reoriented frames. The arterial input functions were corrected for ammonia metabolites, and the myocardial tissue curves were corrected for spillover of activity, partial volume effects, and heterogeneities in the image's spatial resolution introduced during reorientation. Corrections for regional partial volume were based on estimates of the regional myocardial activity thickness derived from reoriented diastolic images of the heart. The myocardial 13N-ammonia kinetics were described with a two-pool compartmental model. Values of regional myocardial blood flow by PET correlated linearly with those by microspheres (slope, 0.94; y intercept, 0.06 ml/min/g; r = 0.93) over a wide range of flows. CONCLUSIONS: Regional myocardial blood flow can be measured accurately and noninvasively from serially acquired and reoriented short-axis 13N-ammonia images, thus overcoming limitations inherent to the use of transaxially acquired images and permitting a more complete evaluation of regional blood flows throughout the left ventricular myocardium.

Ammonia↗
PubMed1999

The effect of surface roughness of microporous membranes on the kinetics of oxygen consumption and ammonia elimination by adherent hepatocytes.

In membrane hybrid liver support devices (HLSDs) using isolated hepatocytes where oxygen is transported only by diffusion to the cells, about 15-40% of the cell mass is likely to be in direct contact with the semipermeable membranes used as immunoselective barriers: quantitative effects of membrane surface properties on the kinetics of hepatocyte metabolic reactions may also affect HLSD performance. In this paper, we report our investigation of the effects of surface morphology of two microporous commercial membranes on the kinetics of oxygen consumption and ammonia elimination by primary hepatocytes in adhesion culture. Isolated rat hepatocytes were cultured on polypropylene microporous membranes with different surface roughness and pore size in a continuous-flow bioreactor whose fluid dynamics was optimized for the kinetic characterization of liver cell metabolic reactions. Collagen-coated membranes were used as the reference substratum. Hepatocyte adhesion was not significantly affected by membrane surface morphology. The rates of the investigated reactions increased with ammonia concentration according to saturation kinetics: the values of kinetic parameters Vmax and K(M) increased as cells were cultured on the membrane with the greatest membrane surface roughness and pore size. For the reaction of oxygen consumption, Vmax increased from 0.066 to 0.1 pmol h(-1) per cell as surface roughness increased from 70 to 370 nm. For the kinetics of ammonia elimination. K(M) increased from 0.23 to 0.32 mM and Vmax increased from 1.49 to 1.79 pmol h(-1) per cell with membrane surface roughness increasing from 70 to 370 nm. Cells cultured on collagen-coated membranes consistently yielded the highest reaction rates. The Vmax values of 0.18 and 2.84 pmol h(-1) per cell for oxygen consumption and ammonia elimination, respectively, suggest that cell functions are also affected by the chemical nature of the substratum.

Ammonia↗
PubMed1967

Studies on the intracerebral toxicity of ammonia.

Interference with cerebral energy metabolism due to excess ammonia has been postulated as a cause of hepatic encephalopathy. Furthermore, consideration of the neurologic basis of such features of hepatic encephalopathy as asterixis, decerebrate rigidity, hyperpnea, and coma suggests a malfunction of structures in the base of the brain and their cortical connections. The three major sources of intracerebral energy, adenosine triphosphate (ATP), phosphocreatine, and glucose, as well as glycogen, were assayed in brain cortex and base of rats given ammonium acetate with resultant drowsiness at 5 minutes and subsequent coma lasting at least 30 minutes. Cortical ATP and phosphocreatine remained unaltered during induction of coma. By contrast, basilar ATP, initially 1.28 +/- 0.15 mumoles per g, was unchanged at 2.5 minutes but fell by 28.1, 27.3, and 26.6% (p < 0.001) at 5, 15, and 30 minutes after NH(4)Ac. At comparable times, basilar phosphocreatine fell more strikingly by 62.2, 96, 77.1, and 71.6% (p < 0.001) from a control level of 1.02 +/- 0.38 mumoles per g. These basilar changes could not be induced by anesthesia, psychomotor stimulation, or moderate hypoxia and were not due to increased accumulation of ammonia in the base. Glucose and glycogen concentrations in both cortex and base fell significantly but comparably during development of stupor, and prevention of the cerebral glucose decline by pretreatment with glucose did not obviate ammonia-induced coma or the basilar ATP fall. These findings represent the first direct evidence that toxic doses of ammonia in vivo acutely affect cerebral energy metabolism and that this effect is preferentially localized to the base of the brain.

Adenosine Triphosphate↗
PubMed1969

Studies with 15N-labeled ammonia and urea in the malnourished child.

Investigations using ammonium citrate-(15)N and urea-(15)N showed that children in the acute stage of kwashiorkor and marasmus receiving a diet of adequate protein content retained a considerable percentage of the label from both compounds. Excretion of both total (15)N and urea-(15)N was subnormal and elimination was virtually completed 36 hr after administration of the isotope. During recovery from kwashiorkor total (15)N excretion had approached normal a month after commencement of rehabilitation. Urea-(15)N excretion was still slightly subnormal after 3 months. In marasmus urea-(15)N formed a normal proportion of total (15)N excretion after 1 month, although total (15)N excretion then was still low. Ammonia nitrogen was retained to a greater extent than urea nitrogen in all cases. As it is known that a considerable amount of urea is degraded to ammonia in the gastrointestinal tract, it seems probable that urea nitrogen became available for use after this degradation. Examination of blood from one marasmic child after feeding ammonia-(15)N and from another after intravenous injection of urea-(15)N showed incorporation of the label into blood cells and plasma proteins. This did not occur in well nourished controls. It is concluded that ammonia and urea as sources of nonessential nitrogen may play an important part in protein metabolism in the malnourished child.

Ammonia↗
PubMed1975

Effect of volume expansion on renal citrate and ammonia metabolism in KCl-deficient rats.

When rats with desoxycorticosterone acetate (DOCA)-induced potassium chloride deficiency are given sodium chloride there is simultaneously a partial correction of metabolic alkalosis and a marked reduction in urinary citrate excretion and renal citrate content. To examine DOCA's role in this phenomenon and to determine how sodium chloride alters renal metabolism, rats were made KC1 deficient using furosemide and a KC1-deficient diet. Renal citrate and ammonia metabolism were then studied after chronic oral sodium chloride administration or acute volume expansion with isotonic mannitol. Although both maneuvers partially corrected metabolic alkalosis, sodium chloride raised serum chloride concentration while mannitol significantly decreased it. Urinary citrate excretion decreased to 10% of control in rats given NaCl and to 50% of control in rats infused with mannitol. The filtered load of citrate was constant or increased indicating increased tubular citrate reabsorption. Renal cortical citrate content also decreased approximately 50%. Renal cortical slices from KCl-deficient rats incubated in low or normal chloride media produced equal amounts of 14CO2 from (1, 5-14C) citrate. In addition, urinary ammonia excretion increased by over 300% in both groups. This occurred in the mannitol group despite increased urinary pH and flow rate indicating a rise in renal ammonia production. It seems that neither DOCA nor an increase in serum chloride concentration explains the experimental results. Rather, it appears that volume expansion is responsible for increased renal tubular citrate reabsorption and renal ammonia production. As these renal metabolic responses ordinarily occur in response to acidosis, the data are consistent with the hypothesis that volume expansion reduces renal cell pH in 3KCl-deficient rats.

Ammonia↗