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PubMed1977

Bicarbonate-induced phosphaturia: Dependence upon the magnitude of phosphate reabsorption.

The acute effect of bicarbonate infusion on inorganic phsophate (Pi) reabsorption was determined in thyroparathyroidectomized (TPTX) rats stabilized on a high phsophorus diet. In the normophosphatemic state, bicarbonate did not affect Pi reabsorption significantly. On the other hand, after hyperphosphatemia was induced by phosphate loading, bicarbonate inhibited Pi reabsorption. In order to determin if eht aboslute level of plasma or filtered Pi was an improtant determinant of this phosphaturic action of bicarbonate during hyperphosphatemia, equivalent rates of Pi reabsorption were achieved after phosphate infusion in TPTX rats previously stabilized on a low dietary phosphorus intake, but at significantly lower plasma Pi concentrations and filtered Pi loads than in their high dietary phosphorus counterparts. Bicarbonate inhibited Pi reabsorption equivalently in both hyperphosphatemic groups, indicating that the magnitude of Pi transport itself was of importance in determining the inhibitory response to bicarbonate. In addition, the results suggest that transport mechanisms for bicarbonate and Pi may interact competitively.

Animals↗
PubMed1996

Capsaicin-sensitive sensory neurons are involved in bicarbonate secretion induced by lansoprazole, a proton pump inhibitor, in rats.

Lansoprazole, a proton pump inhibitor, exerts prominent antiulcer activity via both antisecretory and mucosal protective actions. Although the antisecretory action has been explained by inactivation of (H+, K+)-ATPase in parietal cells, the mode of mucosal protective action remains to be elucidated. In the present study, the effect of lansoprazole on duodenal bicarbonate secretion was studied in anesthetized rats to clarify the mode of the mucosal protective action. Lansoprazole (0.1 mM) applied topically to the duodenum significantly (P < 0.01) increased bicarbonate secretion by 0.36 +/- 0.11 microeq/15 min (21 +/- 5%) compared with the value in the vehicle control. Topical administration of capsaicin (10 mg/ml) in the duodenum and intravenous infusion of vasoactive intestinal peptide (10 micrograms/kg/hr) increased bicarbonate secretion. Five-minute perfusion of the duodenal loop with 100 mM HCl increased bicarbonate secretion. Administration of lansoprazole (0.3 and 1 mg/kg, intravenously) 60 min before luminal acidification enhanced the acid-induced bicarbonate secretion dose-dependently and significantly (P < 0.01). In the capsaicin-pretreated rats, the effects of lansoprazole on basal and acid-induced bicarbonate secretion were significantly (P < 0.05) decreased compared with that of control group. These results indicate that lansoprazole increases basal and acid-induced bicarbonate secretion in the duodenum in rats and that capsaicin-sensitive sensory neurons may be involved in the mode of action for these effects.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed2006

Bicarbonate kinetics in Indian males.

Measurement of rates of in vivo substrate oxidation such as that of glucose, fatty acids and amino acids, are based on tracer (14C or 13C) data, and often depend on the isotopic content of expired CO2. The recovery of tracer-labelled CO 2 generated from the oxidation of 13C labelled substrates may not be 100% over short term. This can lead to underestimation of oxidation rate of substrates, and consequently a correction for the incomplete recovery of tracer has to be applied by the determination of the recovery of 13CO2 in the breath during tracer bicarbonate infusions. We have studied the recovery of tracer-labelled bicarbonate using a bolus administration model, and further characterized kinetics of bicarbonate using a three-compartment model, to assess which compartmental fluxes changed during the change from a fasted state to fed state. Recovery of bicarbonate was lower at 69% and 67% (fasted and fed state) than the value of 71% and 74% found during earlier longer term of continuous infusions. During feeding, there was a 20-fold increase in the flux of bicarbonate between the central compartment and the compartment that was equivalent to the viscera. This study shows that the difference between the fasted and fed state recovery of tracer bicarbonate similar to that obtained with continuous infusions, and that bicarbonate fluxes show large changes between different compartments in the body depending on metabolic state.

Bicarbonates↗
PubMed1981

Photodynamic alteration of cornea endothelium. Relation to bicarbonate fluxes and oxygen concentration.

Corneas were mounted in flux chambers and endothelial bicarbonate fluxes were determined following sensitization of endothelial cells with 5 . 10(-6) M rose bengal and exposure to light. Corneas exposed to light demonstrated an increased passive bicarbonate flux compared to corneas not photosensitized. Active bicarbonate flux was reduced after 5 min of light exposure, but not after 1 min of light exposure. The increase in passive bicarbonate flux was prevented by the addition of 200 microgram/ml catalase to the bathing solution; however, catalase had no effect on the photodynamic alteration of active flux. Neither 10 mM ascorbic acid nor 1.012 gram/l glutathione prevented the photodynamically induced increase in passive flux. Perfusion of corneas with 5 . 10(-6) M rose bengal dissolved in a sucrose-substituted Krebs-Ringer bicarbonate solution with a PO2 of 124 +/- 4.0 mmHg and exposed to light swelled at rates more rapid than corneas treated in a similar fashion but perfused with a solution with a PO2 of 20 +/- 4.6 mmHg. This study demonstrated that photodynamically induced corneal endothelial cell alteration results in increased passive bicarbonate flux, a time-dependent decrease in active bicarbonate flux, is oxygen dependent, and is at least in part secondary to H2O2 produced by the dismutation reaction of the superoxide free radical.

Animals↗
PubMed1992

In vivo bicarbonate secretion by human esophagus.

The capacity of the human esophagus to secrete bicarbonate was studied in vivo in 10 healthy subjects. A 10-cm segment of the lower esophagus was isolated between two balloons, and the segment was perfused with an unbuffered isotonic saline solution (pH 7) for 30 minutes. The perfusate was collected, pooled, and analyzed for bicarbonate using a sensitive back-titration method. Measurements of aspirate amylase and salivary amylase and bicarbonate permitted correction of perfusate bicarbonate values for contamination by swallowed saliva. The esophagus of all 10 subjects were found to secrete bicarbonate in amounts ranging from 10 to 274 microEq/30 min (average, 78 microEq/30 min); based on in vitro studies, these amounts of bicarbonate were shown to be capable of neutralizing enough residual acid from an episode of reflux to increase pH from 2.5 almost to neutrality (pH 6-7). These findings document the presence within the human esophagus of an additional mechanism for defense against (acid) reflux damage, namely, through enhanced luminal acid clearance by the secretion of bicarbonate ions.

Adult↗
PubMed1994

Role of bicarbonate in blood flow-mediated protection and repair of damaged gastric mucosa in the cat.

BACKGROUND/AIMS: The hyperemic response after superficial gastric mucosal damage is essential for repair of the mucosa. Only indirect evidence suggests that this is caused by supply of bicarbonate. Therefore, this study tested the effect of maintaining the availability of bicarbonate after prevention of the hyperemic response after damage by 2 mol/L NaCl. METHODS: Celiac artery flow was reduced, as monitored by Doppler ultrasonography, by gradual constriction of the vessel after mucosal damage. Saline (pH 1.0) was perfused through the stomach lumen and thereafter through a closed chamber with pH and PCO2 electrodes. RESULTS: Exposure to 2 mol/L NaCl produced a marked increase of mucosal blood flow as measured by microspheres (P < 0.025) and a high degree of mucosal restitution 90 minutes after damage as judged by microscopy, whereas prevention of the hyperemic response caused extensive erosions and much less restitution (P < 0.001). The latter effect was completely counteracted by intravenous bicarbonate. High blood concentration of bicarbonate increased luminal release of bicarbonate, whereas high mucosal blood flow did not. CONCLUSIONS: These data show that bicarbonate is an important factor in blood flow-mediated protection and repair of damaged gastric mucosa and suggest that concentration gradients are the major determinants for transport of bicarbonate across the damaged and restituted mucosa.

Animals↗
PubMed1995

Histamine inhibits prostaglandin E2-stimulated rabbit duodenal bicarbonate secretion via H2 receptors and enteric nerves.

BACKGROUND/AIMS: The gastroduodenal epithelium is protected from acid peptic damage by an adherent mucus-bicarbonate layer. Bicarbonate is secreted by the surface epithelial cells into this mucus layer. Patients with duodenal ulcer disease have impaired proximal duodenal bicarbonate secretion. Mast cells, present in large numbers in the duodenal mucosa, release a number of inflammatory mediators, including histamine. Release of such mast cell mediators has been implicated in ulcer disease. In this study, the ability of histamine to regulate bicarbonate secretion was examined. METHODS: Bicarbonate secretion by rabbit proximal duodenal mucosa was examined in vitro, and the effects of histamine, its agonists, and its antagonists were studied. RESULTS: Histamine essentially eliminated prostaglandin E2-stimulated duodenal mucosal bicarbonate secretion, an effect reversed both by the neurotoxin, tetrodotoxin, and the histamine H2-receptor antagonist, cimetidine, as well as reproduced by the H2-receptor agonist, dimaprit. CONCLUSIONS: In addition to the stimulatory action of histamine on gastric acid secretion, histamine expresses an additional antidefensive action by inhibiting prostaglandin E2-stimulated duodenal epithelial bicarbonate secretion. This effect of histamine is likely mediated via H2 receptors located on enteric nerves.

Animals↗
PubMed2004

Bicarbonate and its role in mammalian sperm function.

This paper deals with the effects of bicarbonate induced signaling pathways on plasma membrane lipid organization and downstream protein signaling, and their role in sperm-egg interactions. It also provides an overview of results that indicate that bicarbonate responses are not related to cell death or apoptosis. The information presented shows that only those sperm cells that have functionally completed maturation in the epididymis are sensitive to bicarbonate whereas immature sperm fail to respond to this physiological challenge. Therefore, it is important to selectively analyze the responsive sperm subpopulations when studying sperm capacitation. Moreover, bicarbonate induced signaling responses differ within the diverse sperm structures (e.g. the tail versus the head). Consequently, dissecting sperm structures and signaling areas from each other deserves more attention in sperm capacitation research. The information discussed was obtained from a variety of mammalian species but the basic bicarbonate-mediated sperm responses are similar in most Eutherian species despite some species to species variations (most notably in kinetics rather than the sequence of events). The objective of the paper is to provide a comparative experimental overview of bicarbonate mediated sperm capacitation in the hope that this information will lead to a better understanding of the complex biochemical nature of the involvement of bicarbonate in mammalian sperm capacitation.

Acrosome Reaction↗
PubMed2004

Protease-activated receptor-2 regulates bicarbonate secretion by pancreatic duct cells in vitro.

BACKGROUND: Pancreatic duct cells (PDCs) are responsible for bicarbonate production by the pancreas. The trypsin-sensitive protease-activated receptor (PAR-2), also known as the trypsin receptor, is highly expressed in the pancreatic duct system and has been shown to regulate PDC ion transport. The possible role of this receptor on bicarbonate secretion, the central function of duct cells, is unknown. We hypothesize that PAR-2 may regulate pancreatic bicarbonate secretion during times of inappropriate pancreatic enzyme activation. METHODS: To study this hypothesis in vitro, explants of the bovine main pancreatic duct were isolated and maintained in primary culture. They were then mounted in Ussing chambers, and bicarbonate secretion was determined with an autoburette titration. The response to luminal or serosal trypsin (10 micromol/L) and the synthetic trypsin receptor activating peptide (TRAP) (30 micromol/L) on spontaneous and secretin-stimulated bicarbonate secretion (10 nmol/L) was examined. RESULTS: Serosal trypsin had no effect. Both luminal trypsin and TRAP significantly reduced the spontaneous bicarbonate secretion observed at luminal pH 7.4 (2.8 +/- 0.2 - 0.4 +/- 0.1 micromol/hr/cm(2) and 4.0 +/- 1.2 - 1.6 +/- 0.4 micromol/hr/cm(2), respectively) in a reversible manner. Baseline bicarbonate secretion at luminal pH 8.0 was reduced by trypsin and TRAP, but the increase in response to secretin stimulation observed with controls was unaffected. CONCLUSIONS: PAR-2 activation may be the mechanism by which pancreatic juice secretion is inhibited during pancreatitis. We suggest that pharmacologic activation of PAR-2 receptors could suppress pancreatic exocrine secretion and thus serve as a potential agent in the treatment and prevention of pancreatic fistulas.

Animals↗
PubMed1998

Inhibition of rabbit duodenal bicarbonate secretion by ulcerogenic agents: histamine-dependent and -independent effects.

BACKGROUND & AIMS: The gastroduodenal epithelium is protected from acid-peptic damage, in part, by its ability to secrete bicarbonate. Patients with duodenal ulcer disease have impaired proximal duodenal mucosal bicarbonate secretion. We have shown in vitro that histamine inhibits prostaglandin-stimulated bicarbonate secretion in rabbit duodenal mucosa via histamine H2 receptors and enteric nerves. In this study we examined whether the proulcerogenic compounds aspirin or ethanol regulate duodenal bicarbonate secretion and the involvement of histamine. METHODS: Bicarbonate secretion by rabbit proximal duodenal mucosa was examined in vitro in Ussing chambers. RESULTS: Aspirin and ethanol decreased basal and prostaglandin-stimulated bicarbonate secretion; the latter effect was specific for prostaglandin. The inhibitory effects of the two ulcerogenic compounds were at least additive. Ranitidine and tetrodotoxin abolished the inhibitory effects on stimulated, but not basal, secretion. Aspirin and ethanol also induced release of duodenal histamine. CONCLUSIONS: Aspirin and ethanol act by two distinct pathways to impair duodenal bicarbonate secretion. Both agents inhibit basal secretion via a histamine-independent and neurally independent pathway while they inhibit prostaglandin E2-stimulated secretion via histamine release, likely from mast cells, and actions on enteric nerves. Our findings may be of relevance to the understanding and potential treatment of nonsteroidal anti-inflammatory drug-associated mucosal injury.

Animals↗
PubMedDate not supplied

Retinal pigment epithelial origin of bicarbonate response.

The mechanisms of the bicarbonate-induced decrease in the ocular standing potential (bicarbonate response) were investigated in the cat. An intravenous infusion of 1.4% sodium bicarbonate solution caused a decrease in the standing potential. A high-bicarbonate solution decreased or increased the potential across the retinal pigment epithelium-choroid tissue of the excised cat eye when applied basally or apically, respectively, but did not affect the potential across the anterior portion of the excised eye or across the isolated neural retina. A high-bicarbonate solution principally depolarized the apical membrane of the retinal pigment epithelium (RPE) when applied basally, and hyperpolarized it when applied apically. These results suggest that the bicarbonate response in the cat is primarily due to the effects of an increase in bicarbonate concentration on the basal membrane of the RPE.

Animals↗
PubMed1996

Sodium bicarbonate in cardiac arrest: a reappraisal.

The routine use of sodium bicarbonate in patients with cardiac arrest has been discouraged, with the benefit of outcome evaluation. Current recommendations include an elaborate stratification of circumstances in which bicarbonate is to be used. The physiological and clinical aspects of bicarbonate administration during cardiopulmonary resuscitation in animal and human studies were reviewed. The onset of significant acidemia or alkalemia is associated with adverse system specific effects. The administration of bicarbonate may mitigate the adverse physiological effects of acidemia, improve response to exogenously administered vasopressor agents, or simply increase venous return due to an osmolar effect, resulting in increased coronary perfusion pressure. Likewise, bicarbonate may have adverse effects in each of these areas. The preponderance of evidence suggests that bicarbonate is not detrimental and may be helpful to outcome from cardiac arrest. An objective reappraisal of the empirical use of bicarbonate or other buffer agents in the appropriate "therapeutic window" for cardiac patients may be warranted.

Acid-Base Equilibrium↗
PubMed1998

Hypothermic preservation of isolated rat lungs in modified bicarbonate buffer, EuroCollins solution or St Thomas' Hospital cardioplegic solution.

OBJECTIVES: Inadequate preservation solutions limit lung storage times and, consequently, transplant programs. To address this problem we established an isolated, ventilated and perfused rat lung preparation. Here we report the effects of hypothermic storage in EuroCollins solution, St Thomas' Hospital cardioplegic solution and a modified bicarbonate buffer solution. METHODS: Lungs from male Wistar rats (230-330 g) were perfused via the pulmonary artery with modified bicarbonate buffer (37 degrees C, 15 ml/min, constant flow) and ventilated by positive pressure (tidal volume:1.6-1.8 ml, 80 breaths/min). Vascular resistance (pulmonary artery pressure:perfusate flow ratio) and airways compliance (tidal volume:tracheal pressure ratio) were measured. After a control perfusion period (20 min), lungs were flushed with, then immersed in, bicarbonate buffer (4 degrees C) for varying periods (0-24 h). After storage, lung function was assessed during 20 min reperfusion. Having established a suitable period for study, storage in EuroCollins, St Thomas' Hospital cardioplegic solution or bicarbonate buffer were compared. RESULTS: Pulmonary compliance (ml/cmH2O) was significantly (P < 0.05) reduced in lungs stored for 6 h in modified bicarbonate buffer (0.026 +/- 0.008), EuroCollins solution (0.013 +/- 0.002) or St Thomas' Hospital solution (0.025 +/- 0.005) compared to unstored lungs (0.068 +/- 0.007). Vascular resistance, (1.32 +/- 0.13 cmH2O/ml per min) in unstored lungs, was similar in lungs stored in St Thomas' Hospital solution but increased significantly in lungs stored in modified bicarbonate buffer (3.22 +/- 0.78 cmH2O/ml per min) or EuroCollins solution (4.66 +/- 0.57 cmH2O/ml per min). CONCLUSIONS: Hypothermic storage of rat lungs for 6 h in modified bicarbonate buffer or St Thomas' Hospital solution causes less increase in vascular resistance on reperfusion than EuroCollins solution.

Animals↗
PubMed2003

Use of a physiologic bicarbonate buffer system for dissolution characterization of ionizable drugs.

PURPOSE: The aim of this study was to examine if sparging with CO2(g) could be used to establish stable biorelevant bicarbonate buffers, in aqueous medium, for use in dissolution characterization of low-solubility ionizable drugs. METHODS: Preparation of the bicarbonate-containing dissolution medium was monitored by use of a commercially available fiberoptic probe to measure the concentration of dissolved CO2(aq). Intrinsic dissolution measurements at 100 rpm, 37 degrees C for indomethacin and dipyridamole were performed using a rotating disk and UV detection at pH 6.8 and 5.0 in a USP dissolution vessel apparatus. RESULTS: Indomethacin dissolution at pH 6.8 was significantly impacted by the concentration of CO2(g) in the sparging gas. Dipyridamole flux at pH 6.8 was independent of buffer species or buffer concentrations studied. However, dipyridamole dissolution at pH 5 was also a strong function of the concentration of CO2(g) in the sparging gas. CONCLUSIONS: Stable bicarbonate biorelevant buffers could be established to perform intrinsic dissolution rate determinations for indomethacin and dipyridamole as long a continuous gas sparging of CO2(g) was used. Depending of the pH of the dissolution medium, the intrinsic dissolution rates of both indomethacin and dipyridamole were affected by the bicarbonate concentration. Sparging with CO2(g) to create physiologic buffers has a unique advantage over conventional buffers in that gas sparging serves as a continuous source of bicarbonate buffer species. This advantage was demonstrated by performing dissolution experiments at pH values typically associated with the fed state (pH 5) and applying relatively low CO2(g) pressures, resulting in bicarbonate concentrations less than 0.5 mM. It was demonstrated that CO2(g) sparging at a pH consistent with the fed state created an in-situ bicarbonate buffer at low concentrations, which had a significant impact on the dissolution of a basic drug such as dipyridamole.

Bicarbonates↗
PubMed2002

Bicarbonate attenuates intracellular acidosis.

BACKGROUND: This study was prompted by concern that administration of bicarbonate for correction of lactate acidosis aggravates a low intracellular pH (pHi). In healthy subjects we evaluated skeletal muscle pHi using 31P-magnetic resonance spectroscopy during 5-minute rhythmic handgrip to provoke intracellular acidosis. METHODS: Subjects were randomized to treatment with bicarbonate or saline infused intravenously in a cross-over study design with 1 h between trials. RESULTS: In response to rhythmic handgrip, muscle venous O(2) hemoglobin saturation decreased from 51 +/- 4% to 36 +/- 2% and lactate increased from 1.0 +/- 0.1 to 4.9 +/- 0.5 mmol/l with a reduction in pH from 7.43 +/- 0.01-7.23 +/- 0.01 (P<0.05). pHi decreased from 7.06 +/- 0.02-6.36 +/- 0.08 (P<0.05). Infusion of bicarbonate increased the arterial blood concentration from 26 +/- 1 to 39 +/- 1 mmol/l (P<0.05). The arterial CO(2) partial pressure decreased from 5.6 +/- 0.2 to 5.2 +/- 0.3 kPa during rhythmic handgrip, whereas it increased to 5.9 +/- 0.2 kPa (P<0.05) during infusion of bicarbonate. Bicarbonate treatment also increased pH of arterial and venous blood (7.55 +/- 0.01 vs. 7.44 +/- 0.02 and 7.31 +/- 0.01 vs. 7.23 +/- 0.02, respectively; P<0.05). In the last min of rhythmic handgrip the decrease in pHi was attenuated by the administration of bicarbonate (6.60 +/- 0.11 vs. 6.40 +/- 0.12; P<0.05). CONCLUSION: During exercise-induced metabolic acidosis, intravenous administration of bicarbonate increased the buffering capacity of blood and attenuated the decrease in intracellular muscle pH, although there was a small increase in the arterial carbon dioxide pressure.

Acidosis↗
PubMed1977

Renal response to phosphorus deprivation: effect of the parathyroids and bicarbonate.

Plasma inorganic phosphate (Pi) and Pi reabsorption were compared in intact and chronically thyroparathyroidectomized (TPTX) rats stabilized on a high or low-phosphorus diet after volume expansion with equivalent sodium bicarbonate or sodium chloride. Phosphate infusion after sodium chloride-loading resulted in greater hyperphosphatemia and diminished phosphaturia in TPTX rats than intact high-phosphorus rats. After sodium bicarbonate-loading, however, there was no difference between intact and TPTX high-phosphorus animals because bicarbonate inhibited Pi reabsorption extensively in both. In contrast, phosphate infusion after sodium chloride-loading in phosphorus-deprived rats elicited greater degrees of hyperphosphatemia and increased Pi reabsorption, irrespective of the presence or absence of the parathyroids. Sodium bicarbonate-loading inhibited Pi reabsorption significantly less in phosphorus-deprived rats than in high-phosphorus animals. Paradoxically, this inhibitory effect of bicarbonate in phosphorus depletion was greater in TPTX rats than in intact animals. Therefore, the presence of the parathyroids did not interfere with Pi reabsorption during phosphate infusion in sodium bicarbonate-loaded phosphorus-deprived rats. Sodium bicarbonate-loading interfered with Pi reabsorption most prominently in phosphorus-deprived rats when the parathyroids were absent.

Animals↗
PubMed1982

Effect of calcium and phosphate on bicarbonate and fluid transport by proximal tubules in vitro.

Previous studies in living animals have suggested that variations in the serum concentrations of calcium and phosphate directly affect renal tubular bicarbonate transport. To examine this area more directly, we measured the bicarbonate and the fluid transport in isolated rabbit proximal convoluted and straight tubules perfused in vitro. The concentration of calcium in the perfusate was varied between 0 and 5 mM and in the bath between 0.5 and 5 mM. In proximal convoluted tubules, 5 mM calcium in the perfusate and bath caused a significant increase in the rate of bicarbonate absorption, and removal of calcium from the perfusate inhibited both bicarbonate and fluid absorption. The concentration of phosphate in the perfusate and the bath was varied from 0.25 to 5 mM. In both convoluted and straight tubules, there was no significant change in bicarbonate or fluid absorption with changes in the ambient phosphate concentration. We conclude that changes in calcium concentration have significant effects on bicarbonate transport by proximal convoluted tubules but that wide variations in the concentration of phosphate have no significant effect on bicarbonate, sodium, or fluid transport by proximal tubules in vitro.

Absorption↗
PubMed1985

Net tubular secretion of bicarbonate by the alligator kidney. Antimammalian response to acetazolamide.

Net tubular secretion of bicarbonate by the alligator kidney was demonstrated during acute clearance experiments where the animals were infused with an isosmotic solution of one-half 5% mannitol and one-half 0.9% NaCl. Tubular secretion of bicarbonate averaged 3.38 mumoles/min in animals with a mean wt of 1.0 kg. During these experiments, mean tubular secretion of urate was 0.51 mumole/min and urinary ammonia excretion was 4.3 mumoles/min. Urinary pNH3 was high and ranged from 22,231 to 41,223 mm Hg X 10(-6). The administration of acetazolamide 25 mg/kg resulted in abolition of bicarbonate secretion, which was replaced by bicarbonate reabsorption. At the same time, the tubular secretion of urate fell by 70% and the excretion of ammonia fell by 77%. This is the first time that net tubular secretion of bicarbonate is demonstrated in a living animal. Acetazolamide has an antimammalian effect. It is proposed that the alligator that lives with a low plasma bicarbonate concentration (10 mM) possesses a kidney in which the renal tubular cells secrete bicarbonate in the tubular lumen and hydrogen at the peritubular site, in contrast to that which takes place in mammalia and other animal species.

Absorption↗