Acute Metabolic Alkalosis Research Articles

Effects of acute acid-base disturbances on renal tubule reabsorption of magnesium in the rat.

The effects of acute metabolic and respiratory acidosis and acute metabolic alkalosis on magnesium excretion and on fractional magnesium delivery to the end-accessible proximal tubule of the superficial nephron and the end-descending limb of the juxtamedullary nephron were examined by micropuncture in anesthetized thyroparathyroid-intact rats. Compared with normal control rats, acute metabolic acidosis (HCl infusion) did not produce any significant change. Acute respiratory acidosis (15% CO2 in inspired air) significantly increased the absolute but not the fractional excretion of magnesium and did not alter fractional delivery of magnesium to the end-accessible superficial proximal tubule or juxtamedullary end-descending limb. Acute metabolic alkalosis (NaHCO3 infusion) significantly reduced absolute and fractional magnesium excretion and fractional magnesium delivery to the end-descending limb of the juxtamedullary nephron but did not affect fractional magnesium delivery to the end-accessible proximal tubule of the superficial nephron. Tubule fluid-to-ultrafilterable magnesium ratio was a function of tubule fluid-to-plasma inulin ratio in the end-descending limb when all groups were combined. These results suggest that although acute metabolic or respiratory acidosis has no significant effect, acute metabolic alkalosis enhances magnesium reabsorption in the juxtamedullary proximal nephron--possibly in the pars recta.

Effects of pH on potassium transport by renal distal tubule.

To determine the relative importance of plasma and luminal pH changes as factors regulating potassium secretion by rat distal tubule, superficial tubules were continuously microperfused in vivo. The effects of changes in plasma pH were examined by producing acute systemic metabolic acidosis or alkalosis and holding luminal flow rate, solute composition, and pH constant by microperfusion. Alternatively, the effect of luminal solution pH was evaluated by microperfusing tubules with solutions buffered to either pH 6.5 or 8.0 at constant systemic acid-base balance. Net transport of Na and K and the pH of the luminal fluid were measured. Results showed that metabolic acidosis inhibited and metabolic alkalosis stimulated potassium secretion. Increased luminal fluid pH, in contrast, did not stimulate potassium transport. In experiments in which metabolic acidosis produced a diuresis, urinary potassium excretion was enhanced compared with hydropenic controls. Free-flow micropuncture studies revealed that the rate of fluid delivery to the distal tubule was 45% greater during acidosis compared with control and that potassium secretion increased in both the distal and collecting tubule. Since the rate of fluid delivery is a potent stimulus of potassium secretion in the distal tubule, it is concluded that the stimulus of increased delivery of fluid, observed in free-flow conditions, masked the inhibitory effect of acidosis on potassium transport. Potassium transport by the distal tubule, during acid-base disorders, is regulated by plasma pH and the rate of delivery of fluid but is not stimulated by alkalinization of the luminal fluid.

Intracellular element concentrations of renal tubular cells during acute metabolic alkalosis

Intracellular element concentrations of renal tubular cells during acute metabolic alkalosis

Changes in brain surface pH during acute isocapnic metabolic acidosis and alkalosis

It has been thought that the blood-brain barrier is relatively impermeable to changes in arterial blood H+ and OH- concentrations. We have measured the brain surface pH during 30 min of isocapnic metabolic acidosis or alkalosis induced by intravenous infusion of 0.2 N HCl or NaOH in anesthetized dogs. The mean brain surface pH fell significantly by 0.06 and rose by 0.04 pH units during HCl or NaOH infusion, respectively. Respective changes were also observed in the calculated cerebral interstitial fluid [HCO-3]. There were no significant changes in cisternal cerebrospinal fluid acid-base variables. It is concluded that changes in arterial blood H+ and OH- concentrations are reflected in brain surface pH relatively quickly. Such changes may contribute to acute respiratory adaptations in metabolic acidosis and alkalosis.

Acetazolamide in the Treatment of Ventilatory Failure Complicating Acute Metabolic Alkalosis

Acetazolamide in the Treatment of Ventilatory Failure Complicating Acute Metabolic Alkalosis

Effect of acute metabolic alkalosis and acidosis on intestinal electrolyte transport in vivo.

The effects of acute metabolic alkalosis and acidosis on intestinal electrolyte transport were studied in adult Sprague-Dawley rats. Animals were made alkalotic or acidotic by gavage feeding of 1 M solutions of NaCl (pH = 7.42), NaHCO3 (pH = 7.52), NH4Cl (pH = 7.18), or 0.75 M (NH4)2SO4 (pH = 7.21). After 1-3 h, animals were anesthetized and prepared for in vivo perfusion of the jejunum, ileum, and colon. The jejunum exhibited increased net potassium absorption in alkalosis and decreased potassium absorption in acidosis. In the ileum, net sodium absorption and potassium secretion were decreased, and bicarbonate secretion was increased in alkalosis, and opposite effects were observed in acidosis. The ileal lumen minus blood gradient for PCO2 (an index of hydrogen ion secretion) was greater in acidotic than in alkalotic animals. The levels of ileal sodium, bicarbonate, and potassium transport and the PCO2 gradient correlated well with the plasma pH and bicarbonate concentration in individual animals. In the colon, net bicarbonate secretion and chloride absorption increased and potassium secretion decreased in alkalosis, and opposite effects were observed in acidosis. The colonic lumen minus blood PCO2 gradient was not affected by acid-base balance. Colonic bicarbonate transport correlated with the plasma chloride concentration as well as with the plasma pH. The acid-base disorders had no effect on transmural potential difference. These results suggest that acute metabolic alkalosis and acidosis alter sodium and hydrogen ion transport in the ileum and chloride and bicarbonate transport in the colon.

Response of the collecting duct to disturbances of acid-base and potassium balance

With light microscopy and scanning electron microscopy, the epithelium of the collecting duct was examined in rats with acute and chronic acid-base disturbances, hypokalemia, hyperkalemia, and during osmotic diuresis and hydropenia. Acid-base disturbances included acute respiratory acidosis, acute metabolic alkalosis, and chronic metabolic acidosis. Two groups of hypokalemic animals were studied, those with and those without an associated metabolic alkalosis. After the appropriate physiologic data were collected, all kidneys were preserved for morpholigic data were collected, all kidneys were preserved for morphologic evaluation by in vivo intravascular perfusion fixation. The percentage of intercalated cells in the epithelium of the collecting duct in the cortex and outer medulla of each kidney was determined by light microscopic examination of 1-mu-thick Epon sections stained with toluidine blue. Qualitative observations were performed with scanning electron microscopy. Intercalated cells represented 36 to 40% of the epithelial cells forming the collecting duct in the cortex and outer and inner stripes of the outer medulla in control animals during hydropenia and during mild osmotic diuresis. No experimental condition studied was found to influence significantly the actual or relative number of intercalated cells, or their distribution in the collecting duct. The hypertrophy of both principal cells and intercalated cells in potassium-depleted animals occurred in both the presence and the absence of metablic alkalosis. Conclusion. Under the conditions of this study, intercalated cells represent a constant population of epithelial cells in the rat collecting duct, and intercalated and principal cells represent distinct cell typs, each defined by rather constant morphologic features. Contrary to previous reports, no evidence was found that a disturbance of hydrogen ion and potassium balance is associated with a conversion of principal to intercalated cells in the collecting duct.

Disposition of intravenous potassium in anuric man: A kinetic analysis

The disposition of a constant-rate (0.3 mEq/kg/hr) intravenous potassium load was studied in anuric, chronic hemodialysis patients. Changes in plasma potassium concentration could be adequately described by a two-compartment kinetic model under both isohydric conditions and during acute metabolic alkalosis. From 63 to 92% of the infused potassium left the extracellular fluid (ECF) in isohydric studies, and from 73 to 97% left the ECF in alkalanizing studies. Cellular uptake of the infused potassium was less when the plasma potassium concentration was higher. Plasma aldosterone levels rose but insulin levels did not increase during infusions. In a juvenile-onset diabetic subject, the impairment of cellular potassium uptake at higher plasma potassium was magnified so that infused potassium was virtually confined to the ECF compartment until exogenous insulin was given. This implies a permissive rather than a regulatory role for endogenous insulin in facilitating cellular entry of excess potassium.

Stimulation of renin by acute selective chloride depletion in the rat.

To determine whether acute chloride depletion per se stimulates renin, we produced selective chloride depletion without sodium depletion in rats by peritoneal dialysis (PD) against 0.15 M NaHCO3 or 0.15 M NaNO3. Control rats were dialyzed against 0.15 M NaCl. Plasma renin activity (PRA) was measured before (PRA1) and 105 minutes after (PRA2) PD. Plasma volume was expanded after PD by infusion of salt-free albumin and was measured immediately after PRA2 by [131I]albumin. In experiment 1, rats were prepared on a normal diet. PRA2 (7.0 +/- 1.0 ng/ml per hr, mean +/- SEM) was increased (P less than 0.05) over PRA1 (4.7 +/- 0.7 ng/ml per hr) in Cl-depleted but not in control rats (PRA1 = 5.3 +/- 0.7, PRA2 = 6.1 +/- 0.7, P = NS). In experiment 2, to produce greater chloride depletion, all rats were prepared for 2 weeks on a low salt diet. PRA2 (47 +/- 5 ng/ml per hr) was increased as compared to PRA1 (24 +/- 2 ng/ml per hr, P less than 0.005) in the Cl-depleted group but not in the control group (PRA1 = 24 +/- 3, PRA2 = 27 +/- 6 ng/ml per hr, P = NS). Serum potassium and final plasma volume were slightly but not significantly lower than controls in these Cl-depleted rats. To exclude an additive effect of these two stimuli for renin, in experiment 2a we infused chloride-depleted rats with three times as much albumin as controls and with KHCO3, 100 mEq/liter. Despite volume expansion and potassium loading, PRA2 (41 +/- 6 ng/ml per hr) was significantly elevated as compared to PRA1 (25 +/- 4 ng/ml per hr, P less than 0.01). Since acute metabolic alkalosis also was present in all Cl-depleted renin-stimulated rats, an additional group (2b) was dialyzed against 0.15 M NaNO3; final plasma arterial pH (7.43) was not different from controls (7.42). Nevertheless, PRA2 levels again were higher (36 +/- 6 ng/ml per hr, P less than 0.05) as compared to PRA1 (23 +/- 4 ng/ml per hr). In all experiments, arterial blood pressure, glomerular filtration rate, and filtered sodium load were not different. Free water reabsorption was lower in Cl-depleted than in control rats. We conclude that acute selective chloride depletion per se is a potent stimulus for renin release.

PH and bicarbonate effects on mitochondrial anion accumulation. Proposed mechanism for changes in renal metabolite levels in acute acid-base disturbances.

Mitochondria from rabbit and dog renal cortex were incubated with 1 mM (14)C-weak acid anions in media containing low (10 mM) or high (40 mM) concentrations of bicarbonate and the steady-state accumulation of labeled anion in the matrix was measured. In the absence of an energy source, no concentration of (14)C-anion in the mitochondrial matrix space was present, but the anion concentration was significantly higher at low- than at high-bicarbonate concentration. Addition of an energy source, usually ascorbate plus tetramethyl-p-phenylenediamine, led to increases in matrix space anion levels and to accentuation of the difference in anion uptake between low- and high-bicarbonate media, so that two to four times as much anion was present at low- than at high-bicarbonate concentrations. The anions affected included substrates for which inner membrane carriers are present in mitochondria, such as citrate, alpha-ketoglutarate, malate, and glutamate, as well as substances which diffuse passively across the inner membrane such as acetate and formate. When a nonbicarbonate medium buffered with Hepes was used, pH change did not alter anion uptake although anion concentrations exceeding those in the medium still developed when an energy source was present. The difference in mitochondrial anion accumulation between low- and high-bicarbonate levels diminished with decreasing temperature or with increasing anion concentration in the medium. Estimation of intramitochondrial pH with [(14)C]5,5-dimethyl-oxazolidine-2,4-dione showed that the pH gradient across the inner mitochondrial membrane was significantly greater with 10 than with 40 mM bicarbonate in the medium.A hypothesis is described that relates this effect of pH and bicarbonate on mitochondrial anion accumulation to the very rapid changes in substrate levels in renal cortex, which develop when acute metabolic acidosis or alkalosis is produced in the intact animal. It is suggested that an abrupt fall in systemic pH and bicarbonate is associated with a shift in substrate in renal cortex out of the cytoplasm and into mitochondria, where some of the added substrate is metabolized. Reduction in the size of the cytoplasmic pool of substrate occurs with relatively little accompanying change in the size of the mitochondrial pool, thus causing a net reduction in the total tissue pool. This mechanism accounts for the reduction in tissue levels of many mitochondrial substrates observed acutely in metabolic acidosis. In metabolic alkalosis, reversal of these effects leads to expansion of the cytoplasmic pool, thereby resulting in the rise in tissue levels of substrates which occurs in this condition.

Determination of liver intracellular pH in vivo and its homeostasis in acute acidosis and alkalosis.

An in vivo method is presented for the determination of liver intracellular pH (pHi) using [14C]dimethadione (DMO) in dogs. This method differs from those previously published in that hepatic venous and portal venous blood pH were selected as the extracellular reference pH, and liver blood space corrections are applied to whole liver tissue [14C]DMO activity. Using these corrections, a normal liver pHi of 6.99 +/- 0.03 (SE) was obtained. During acute metabolic acidosis and alkalosis, as well as during acute respiratory acidosis and alkalosis, the liver pHi remained normal; metabolic acidosis was 7.04 +/- 0.04; metabolic alkalosis was 6.92 +/- 0.08; respiratory acidosis was 6.98 +/- 0.04; and respiratory alkalosis was 7.00 +/- 0.10. None of these values was significantly different from normal (P greater than 0.05). Changes in intracellular bicarbonate and lactate appeared to account in part for the observed stability of the liver pHi despite acute manipulations resulting in a range of pH values between 7.09 and 7.63 in arterial blood.

Effects of Acetazolamide and Changes of Acid-Base Balance on the Content of Cyclic Nucleotides in the Rat Kidney

Changes in tissue levels of cyclic adenosine 3':5'-monophosphate (cAMP) and cyclic guanosine 3':5'-monophosphate (cGMP) in the rat kidney in response to acid-base changes and administration of acetazolamide were measured. cAMP was determined according to the method described by Gilman and cGMP by radioimmunoassay. 1 mg/kg acetazolamide increased bicarbonate excretion 100-fold over the control values to 2.52 +/- 0.5 mEq/min (mean +/- SEM; n = 6), but did not influence cGMP and cAMP tissue content. 10 and 100 mg/kg acetazolamide increased cGMP tissue levels to 0.277 +/- 0.048 and 0.482 +/- 0.07 pmol/mg dry weight in comparison to 0.192 +/- 0.04 in the controls, whereas no changes in cAMP levels occurred. Chronic as well as acute metabolic alkalosis induced an increase of cGMP levels (0.26 +/- 0.03 and 0.29 +/- 0.06 pmol/mg), whereas chronic metabolic and acute respiratory acidosis lowered cGMP levels to 0.14 +/- 0.02 and 0.13 +/- 0.02 pmol/mg. cAMP tissue levels were not affected by changes in acid-base balance. The data could suggest that cGMP participates in the regulation of acid-base balance and renal effects of acetazolamide.

Acute and chronic changes in intra- and extracellular potassium and responses to neuromuscular blocking agents.

The effects of acutely induced metabolic and respiratory alkalosis with reduction of serum potassium concentration as well as chronic total body potassium depletion induced by furosemide treatment were evaluated and correlated with alteration of neuromuscular blockade induced by d-tubocurarine, pancuronium, and succinylcholine in 12 mongrel dogs. Acute respiratory and metabolic alkalosis significantly reduced serum potassium by about 26%, while chronic furosemide treatment (1 mg/kg IV daily for 14 +/- 4 days) significantly reduced both serum potassium concentration (4.16 +/- 0.31 to 3.27 +/- 0.14 mEq/L) and skeletal muscle potassium content (80.9 +/- 5.6 to 58.7 +/- 4.1 mEq/kg). Succinylcholine neuromuscular blockages was essentially unchanged by acute respiratory or metabolic alkalosis or by chronic furosemide treatment, except for more rapid onset of blockade when 0.1 mg/kg succinylcholine was administered during metabolic alkalosis. Acute respiratory alkalosis shortened the duration of neuromuscular blockade induced by d-tubocurarine and pancuronium while acute metabolic alkalosis shortened the duration of pancuronium only and had no effect on d-tubocurarine. Chronic furosemide treatment had no effect on either d-tubocurarine or pancuronium neuromuscular blockage. Potassium concentration gradients between the intracellular and the extracellular compartments may be more important than cellular potassium depletion per se in affecting responses to neuromuscular blocking agents such as succinylcholine, d-tubocurarine, or pancuronium. Serum alkalemia and hypokalemia antagonize the duration of the neuromuscular blocking action of d-tubocurarine and pancuronium but not that of succinylcholine.

Acute Metabolic Alkalosis Perpetuating Hypercarbia

Acute Metabolic Alkalosis Perpetuating Hypercarbia

Effects of saline infusion and acute metabolic acidosis and alkalosis on water and electrolyte transport in the human colon.

Both the kidney and colon secrete bicarbonate and transport water and electrolytes. The respective contributions of these two organs to acid-base and electrolyte balance in normal man has thus been studied in eight healthy male volunteers who underwent simultaneous renal clearance studies, and colonic perfusion with a 0.9% saline or 7.2% mannitol solution, during metabolic alkalosis and acidosis, extracellular volume expansion, and control conditions. There was no influence of these acid-base conditions on electrolyte transport in the colon. In the urine, preferential loss of chloride over sodium averaged 81, 143 (P less than 0.001), and 141 (P less than 0.05) muequiv./min, during control, metabolic acidosis, and extracellular volume expansion conditions, respectively. During alkalosis more sodium than chloride was lost (146 muequiv./min) (P less than 0.001). Colonic pH averaged 7.41 during saline and 6.75 (P less than 0.005) during mannitol perfusion. Titratable acid was not produced in the colon during saline perfusion, and averaged 18 muequiv./min during mannitol perfusion. Urinary titratable acid increased from 19 to 25 muequiv./min (P less than 0.01) during volume expansion. With saline perfusion, bicarbonate secretion rate in the colon rose from 249 muequiv./min during control conditions to 289 muequiv./min during metabolic alkalosis (P less than 0.05). More bicarbonate was excreted in the urine during alkalosis when mannitol was introduced in the colon (243 muequiv./min) than when saline was perfused (152 muequiv./min) (P less than 0.05). This study indicates that the response of the human colon is trivial compared with that of the kidney during acute changes in acid-base balance.

Acid-base changes in milk and blood of rats in acidosis and alkalosis.

Lactating white rats (Rattus norvegicus) were subjected to metabolic and respiratory acidosis and metabolic alkalosis. Before and during the various treatments, the acid-base status of heart blood and milk was determined. Acute metabolic acidosis lowered the pH of plasma and milk; Pco(2) and bicarbonate concentrations in plasma were lowered, and in milk Pco(2) was raised and the bicarbonate concentration remained unchanged. Respiratory acidosis and acetazolamide caused a drop in blood pH and in blood and milk bicarbonate concentrations; milk pH remained unchanged, but Pco(2) was raised in both plasma and milk. Acute metabolic alkalosis raised the blood pH and milk Pco(2); plasma Pco(2) and bicarbonate concentrations in blood and milk remained unchanged. The data show that greater changes occur in acid-base parameters of blood than milk when animals are exposed to acidifying and alkalinizing stimuli.

Sodium Bicarbonate and Systemic Hemodynamics in Volunteers Anesthetized with Halothane

The cardiovascular effects of acute metabolic alkalosis (NaHCO3) in normal male volunteers anesthetized with halothane were measured. Pure metabolic alkalosis was studied by maintaning the end-tidal carbon dioxide tension at 40 torr. In each subject, cardiac index increased and total peripheral resistance decreased after each dose of NaHCO3. The increased cardiac index was associated with increased central blood volume, left ventricular minute work index, stroke index, and heart rate. Systolic time intervals showed increased myocardial performance. NaHCO3 administered to volunteers whose hearts were depressed by halothane appeared to cause peripheral vasodilation, volume expansion, and myocardial stimulation. The authors conclude that NaHCO3 administered during halothane anesthesia decreases total peripheral resistance and may lead to severe hypotension.

Compensatory hypoventilation and hypercapnia in primary metabolic alkalosis: Report of three cases

Three patients are described with primary hypokalemic metabolic alkalosis accompanied by marked hypercapnia; arterial carbon dioxide tension (PaCO 2) exceeded 60 mm Hg. In each case, arterial blood gas composition became normal as the alkalosis was corrected with appropriate fluid and electrolyte therapy. “Compensatory” hypoventilation in metabolic alkalosis has rarely been reported in the absence of preexisting lung disease with chronic carbon dioxide retention. Our experience, and review of the few similar reported cases, suggests that dehydration and/or azotemia appear to be necessary for this degree of hypercapnia to occur as a response to metabolic alkalosis. Induction of acute metabolic alkalosis in one patient (after recovery) by rapid infusion of sodium bicarbonate (NaHCO 3) produced no significant change in PaCO 2 or minute ventilation. Hypercapnia, when associated with alkalosis in patients without chronic pulmonary disease, should be recognized as compensatory; rapid reduction in PaCO 2 by mechanical ventilation should be avoided. In these patients, correction of the primary metabolic defect will be accompanied by a secondary decrease in PaCO 2.

Relation of renal gluconeogenesis to ammonia production in the rat.

ARTICLESRelation of renal gluconeogenesis to ammonia production in the ratPC Churchill, and RL MalvinPC Churchill, and RL MalvinPublished Online:01 Feb 1970https://doi.org/10.1152/ajplegacy.1970.218.2.353MoreSectionsPDF (1 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByAmmonia Transporters and Their Role in Acid-Base BalanceI. David Weiner and Jill W. Verlander1 February 2017 | Physiological Reviews, Vol. 97, No. 2Transport and utilization of α-ketoglutarate by the rat kidney in vivo1 January 1989 | Pflügers Archiv - European Journal of Physiology, Vol. 413, No. 3Glucose metabolism in renal tubular functionKidney International, Vol. 29, No. 1Ammonia metabolism during acid-base disturbanceIrish Journal of Medical Science, Vol. 154, No. 7Renal tubular biochemistry during acute and chronic metabolic alkalosis in the dogKidney International, Vol. 27, No. 6Influence of pyruvate on ammonia metabolism by renal cortical mitochondriaKidney International, Vol. 22, No. 3Dissociation between renal gluconeogenesis and ammoniagenesis after acute liver intoxicationToxicology Letters, Vol. 10, No. 4Nephron heterogeneity: gluconeogenesis from pyruvate in rabbit nephron12 November 2001 | FEBS Letters, Vol. 116, No. 2Ammonia production and pathways of glutamine utilization in rat kidney slicesBiochimica et Biophysica Acta (BBA) - General Subjects, Vol. 444, No. 3Renal Metabolic Processes and Acid-Base ChangesMedical Clinics of North America, Vol. 59, No. 3Stimulation of renal gluconeogenesis in methylacetamide diabetesNaunyn-Schmiedeberg's Archives of Pharmacology, Vol. 280, No. 2Metabolic consequences of acid-base disordersKidney International, Vol. 1, No. 5 More from this issue > Volume 218Issue 2February 1970Pages 353-357 Copyright & PermissionsCopyright © 1970 by American Physiological Societyhttps://doi.org/10.1152/ajplegacy.1970.218.2.353PubMed5412447History Published online 1 February 1970 Published in print 1 February 1970 Metrics

Relation of renal gluconeogenesis to ammonia production in the dog.

ARTICLESRelation of renal gluconeogenesis to ammonia production in the dogPC Churchill, and RL MalvinPC Churchill, and RL MalvinPublished Online:01 Jan 1970https://doi.org/10.1152/ajplegacy.1970.218.1.241MoreSectionsPDF (1 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByEffect of hyperketonemia on renal ammonia excretion in manMetabolism, Vol. 35, No. 8Renal tubular biochemistry during acute and chronic metabolic alkalosis in the dogKidney International, Vol. 27, No. 6Regulation of renal ammoniagenesis during acidosis: The pyridine nucleotide hypothesis revisitedLife Sciences, Vol. 27, No. 24Response of the rat and dog kidney to H+ concentration in vitro—A comparative study with slices and tubulesInternational Journal of Biochemistry, Vol. 12, No. 1-2RESPONSE OF THE RAT AND DOG KIDNEY TO H+ CONCENTRATION IN VITRO—A COMPARATIVE STUDY WITH SLICES AND TUBULESRelationship between lactate and glutamine metabolism in vitro by the kidney: Differences between dog and rat and importance of alanine synthesis in the dogKidney International, Vol. 16, No. 4The regulation of renal ammoniagenesis in the rat by extracellular factors. I. The combined effects of acidosis and physiologic fuelsMetabolism, Vol. 27, No. 11Gluconeogenesis and ammoniagenesis in rat kidney: Effect of 3-mercaptopicolinic acid19 October 2001 | FEBS Letters, Vol. 65, No. 2The role of potassium in the control of ammonium excretion during starvationMetabolism, Vol. 25, No. 2Lactic acidosis and renal phosphoenolpyruvate carboxykinase activity during exerciseBiochemical Medicine, Vol. 14, No. 4Effect of starvation on renal metabolism in the ratKidney International, Vol. 7, No. 6Renal Metabolic Processes and Acid-Base ChangesMedical Clinics of North America, Vol. 59, No. 3Role of the kidneys in hyperglycemia provoked by anti-insulin serum in ratsDiabetologia, Vol. 10, No. 2Hyperglutamatemia in primary goutThe American Journal of Medicine, Vol. 54, No. 6Ionic control of renal gluconeogenesis: I. The interrelated effect of calcium and hydrogen ionsBiochimica et Biophysica Acta (BBA) - General Subjects, Vol. 313, No. 1Possible contribution of renal gluconeogenesis to the development of N-monomethylacetamide-induced hyperglycemia in the ratDiabetologia, Vol. 9, No. 2Metabolic consequences of acid-base disordersKidney International, Vol. 1, No. 5Renal Function and Renal MetabolismPediatric Clinics of North America, Vol. 18, No. 2 More from this issue > Volume 218Issue 1January 1970Pages 241-245 Copyright & PermissionsCopyright © 1970 by American Physiological Societyhttps://doi.org/10.1152/ajplegacy.1970.218.1.241PubMed5409882History Published online 1 January 1970 Published in print 1 January 1970 Metrics