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PubMed1981

Inefficacy of bicarbonate infusions on the course of postischaemic acute renal failure in the rat.

Since bicarbonate has been reported to elicit fast recovery from acute renal failure in man, clearance studies were performed to compare the effects of sodium bicarbonate and saline infusion on renal function in postischaemic renal failure in the rat. In a first set of experiments the left kidney and in a second both kidneys were clamped for a period of 45 min and renal function monitored up to 210 min after release of the clamp. Glomerular filtration rate (ml/min) decreased following clamping from (mean values +/- SEM) 1.33 +/- 0.09 to 0.12 +/- 0.02 (saline) or 1.43 +/- 0.1 to 0.08 +/- 0.01 (bicarbonate) in the unilaterally clamped kidney and from 2.94 +/- 0.20 to 0.41 +/- 0.10 (saline) or 2.81 +/- 0.17 to 0.22 +/- 0.03 (bicarbonate) when both kidneys were clamped. Fractional excretion of water and sodium increased to a similar extent in saline and bicarbonate treated animals. Plasma potassium decreased (from 3.37 +/- 0.10 to 2.95 +/- 0.07 [unilaterally clamped kidneys] or from 5.2 +/- 0.4 to 4.4 +/- 0.2 [bilaterally clamped kidneys]) in bicarbonate treated but remained constant in saline treated animals, an effect not related to altered renal potassium excretion. In conclusion, no evidence was found that bicarbonate improves renal function in postischaemic renal failure.

Acute Kidney Injury↗
PubMed1992

Stimulatory effect of bicarbonate on the glycolysis of Actinomyces viscosus and its biochemical mechanism.

The effects of bicarbonate on acid production by 4 human strains of Actinomyces viscosus were estimated under anaerobic conditions. The rate of acid production was accelerated by bicarbonate 3-4 times as much as that without bicarbonate. The analyses of intracellular glycolytic intermediates, NAD and NADH revealed a decrease in NADH:NAD ratio and an increase in the level of 3-phosphoglycerate in the cells when bicarbonate was present. Furthermore, when bicarbonate was available, malate dehydrogenase and fumarate reductase in the succinate pathway were expected to function as NADH-oxidizing enzymes in addition to lactate dehydrogenase. These observations indicate the efficient regeneration of NAD in the presence of bicarbonate. Thus, the stimulation of A. viscosus glycolysis by bicarbonate was thought to stem from the activation of glyceraldehyde 3-phosphate dehydrogenase (G3PDH) by the decrease in the level of NADH, because NADH was a strong inhibitor of G3PDH in this microorganism.

Acetates↗
PubMed1983

Bicarbonate and the pathway of glutamate oxidation in isolated rat-liver mitochondria.

1. The factors affecting the pathway of glutamate oxidation were studied in isolated rat-liver mitochondria in incubations of 2-3 min. 2. It was found that bicarbonate at a physiological concentration has a profound effect on the pathway of glutamate oxidation. Ammonia formation via glutamate dehydrogenase is stimulated by bicarbonate [from 5.48 +/- 0.29 (n = 10) to 9.57 +/- 0.73 (n = 8) nmol X min-1 X mg protein-1], whereas aspartate formation via the transamination pathway is inhibited [from 38.41 +/- 2.24 (n = 9) to 24.56 +/- 3.28 (n = 6) nmol X min-1 X mg protein-1]. 3. Bicarbonate has no effect on the rate of transport of glutamate via the glutamate-hydroxyl translocator. 4. The interaction of bicarbonate with the pathway of glutamate oxidation occurs primarily at the level of succinate dehydrogenase, due to competitive inhibition of the enzyme by bicarbonate. 5. Inhibition by bicarbonate of the transamination pathway leads to a decrease in intramitochondrial 2-oxoglutarate, so that the deamination pathway is stimulated. 6. Using an equation which describes flux through glutamate dehydrogenase kinetically, it could be shown that the bicarbonate-induced decrease in intramitochondrial 2-oxoglutarate quantitatively accounts for the enhanced rate of deamination. 7. It is concluded that in the intact liver flux through glutamate dehydrogenase is sufficient to account for the ammonia formation required for urea synthesis from substrates such as alanine.

Adenosine Diphosphate↗
PubMed1991

Influences of diet, short-chain fatty acids, lactate and chloride on bicarbonate movement across the reticulo-rumen wall of sheep.

Influences of short-chain fatty acids (SCFA), chloride or lactate on net bicarbonate movement were determined in the temporarily isolated and washed reticulo-rumen of sheep used to 100% hay or 81% concentrate diets. Replacement of SCFA by gluconate and mannitol reversed net bicarbonate secretion into net absorption. The reversal of net bicarbonate movement could not be prevented by presence of D/L-lactate. Replacement of chloride in addition to replacement of SCFA enhanced net absorption of bicarbonate. Feeding concentrate diets resulted in an elevation of net bicarbonate secretion and of net SCFA absorption. It is concluded that under the conditions tested net bicarbonate secretion mainly depends on the luminal presence of SCFA. Furthermore, bicarbonate secretion into the reticulo-rumen may be an important factor for alkalizing the rumen contents, especially in sheep adapted to concentrate diets.

Animals↗
PubMed2006

The effect of varying levels of sodium bicarbonate on polychlorinated biphenyl dechlorination in Hudson River sediment cultures.

The addition of different concentrations of sodium bicarbonate had a profound effect on 2,3,4,5-chlorobiphenyl (2,3,4,5-CB) dechlorination in Hudson River sediment cultures. The most extensive dechlorination was observed in cultures to which 100 mg l(-1) bicarbonate was added. Cultures amended with 1000 mg l(-1) bicarbonate had the least extensive dechlorination, with 2,4-CB and 2,5-CB as predominant end-products. A significant loss of total chlorinated biphenyl mass was observed in cultures to which < or = 500 mg l(-1) bicarbonate was added, suggesting that degradation beyond chlorinated biphenyls occurred. The dynamics of acetate formation were different among the treatments, with high acetate concentrations detected throughout the 303-day experiment in cultures to which 1000 mg l(-1) bicarbonate had been added. Sodium bicarbonate addition also had a significant impact on bacterial community structure as detected by polymerase chain reaction-denaturant gradient gel electrophoresis (PCR-DGGE) of 16S rRNA gene fragments. Three putative polychlorinated biphenyl (PCB) dechlorinators were identified; one Dehalococcoides-like population was detected in all enrichment cultures, whereas two Dehalobacter-like populations were only detected in the enrichment cultures with the most extensive dechlorination. These results suggest that the availability of bicarbonate, and potentially sodium, may affect PCB dechlorination in Hudson River sediment and thus need to be taken into consideration when assessing the fate of PCBs or implementing bioremediation.

Acetates↗
PubMedDate not supplied

The effects of equivalent doses of tromethamine or sodium bicarbonate in healthy horses.

OBJECTIVE: To describe the effects of tromethamine, a putative treatment for metabolic acidosis, and to compare its biochemical effects with those of sodium bicarbonate. DESIGN: Randomized intervention study with repeated measures. ANIMALS: 16 healthy horses, 3 to 17 years old, weighing 391 to 684 kg. METHODS: Ten horses received 3 mEq/kg tromethamine and six received 3 mEq/kg sodium bicarbonate. Samples of venous blood and cerebrospinal fluid (CSF) were collected at intervals before and after drug administration. Heart rate and breathing rate were also recorded at intervals. RESULTS: Median standard base excess increased significantly (P < .05) from baseline immediately after both bicarbonate and tromethamine. These increases were not significantly different between treatments. Standard base excess returned toward baseline but remained significantly increased 3 hours after infusion of either treatment. After tromethamine, there was a significant decrease in plasma sodium concentration that lasted for at least 90 minutes. After sodium bicarbonate, no change in plasma sodium concentration was detected. Both sodium bicarbonate and tromethamine increased carbon dioxide tension in venous blood and CSF. Despite venous alkalemia, the pH of CSF decreased after both treatments. CONCLUSIONS: Tromethamine and sodium bicarbonate have similar alkalinizing ability. Tromethamine causes hyponatremia, whereas both tromethamine and sodium bicarbonate increase carbon dioxide tension in venous blood and CSF. CLINICAL RELEVANCE: If hyponatremia, hypercarbia, and acidosis of the CSF occur after tromethamine is given to horses with existing metabolic acidosis, some of the potential advantages of tromethamine may prove theoretical rather than practical.

Acid-Base Equilibrium↗
PubMed2005

Bicarbonate inhibits the growth of Staphylococcus epidermidis in platelet concentrates by lowering the level of non-transferrin-bound iron.

BACKGROUND: Platelet concentrates (PCs) contain non-transferrin-bound iron (NTBI) owing to the displacement of iron from plasma-derived transferrin by citrate. NTBI in the PC medium supports the growth of Staphylococcus epidermidis. The possibilities of lowering the level of NTBI have been studied with the aim to inhibit the growth of S. epidermidis in the PC medium. STUDY DESIGN AND METHODS: NTBI in PC supernatants was determined by a chelation method and by the bleomycin-detectable iron assay. Iron binding by transferrin was determined by spectrophotometry. The growth of inoculated S. epidermidis in PC supernatants was monitored by optical density and determination of viable counts. RESULTS: Bicarbonate enhanced in a dose-dependent manner transferrin iron binding in citrate-containing solutions, including citrated plasma and PAS-II. The use of a modified anticoagulant supplemented with bicarbonate effectively lowered the level of NTBI and inhibited bacterial growth in citrated plasma. Supplementation of bicarbonate to the additive solution to increase the ratio of bicarbonate to citrate in a reconstituted PC medium further inhibited bacterial growth. Maintenance of stable pH and bicarbonate level in the reconstituted medium necessitated storage under 5 percent CO(2). CONCLUSIONS: The relatively low bicarbonate level in PC medium promotes iron displacement by citrate from plasma-derived transferrin. The appearance of NTBI can be decreased and iron-dependent bacterial growth can be inhibited by increasing bicarbonate level in citrated plasma and PC medium. To achieve the same beneficial effect in blood banking, other more practical ways to bind NTBI in a harmless form should be developed.

Bicarbonates↗
PubMed1995

Involvement of renal kallikrein in the regulation of bicarbonate excretion in rats.

1. The experiments reported here were performed to test the hypothesis that renal kallikrein is involved in the regulation of acid-base balance. 2. The bicarbonate concentration and the kallikrein activity in the spontaneously voided urine of conscious rats (experiment 1) were inversely correlated (correlation coefficient (r) = -0.63, P < 0.0001). The correlation was even greater when the urinary bicarbonate concentration was expressed per milligram excreted creatinine (r = -0.74, P < 0.00002). 3. Intravenous injection of the kallikrein inhibitor aprotinin in barbiturate-anaesthetized rats (experiment 2) reduced urinary kallikrein activity (P < 0.05) and increased bicarbonate excretion rate (P < 0.012). 4. Renal arterial infusion of aprotinin in barbiturate-anaesthetized rats (experiment 3) reduced urinary kallikrein activity (120 min, P < 0.01), and increased bicarbonate excretion rate (120 min, P < 0.01). Animals infused with the inhibitor developed a moderate metabolic acidosis (base excess: control, 2.9 +/- 0.7 mM (mean +/- S.E.M.); experimental, -8.1 +/- 0.7 mM; P < 0.05). 5. The bicarbonate concentration of urine fractions obtained after retrograde injection of kallikrein through the ureter into the collecting duct system of barbiturate-anaesthetized rats was lower than that from kidneys administered the vehicle (experiment 4; P < 0.001). A retrograde injection of bradykinin was without effect (experiment 5). 6. We conclude that renal kallikrein is involved in the regulation of urinary bicarbonate excretion. Increased intraluminal activity of the enzyme reduces, and decreased kallikrein activity increases, bicarbonate excretion. The enzyme may be a component of a negative feedback loop controlling the hydrogen ion activity of the extracellular space.

Animals↗
PubMed1963

Studies on immunity in anthrax. XI. Control of cellular permeability by bicarbonate ion in relation to protective antigen elaboration.

Puziss, Milton (Fort Detrick, Frederick, Md.) and Mary B. Howard. Studies on immunity in anthrax. XI. Control of cellular permeability by bicarbonate ion in relation to protective antigen elaboration. J. Bacteriol. 85:237-243. 1963.-No elaboration of Bacillus anthracis protective antigen was demonstrated after addition of bicarbonate to cultures incubated 42 hr in a bicarbonate-free medium. Antigen accumulation in culture filtrates was greater if the bicarbonate was added to these cultures early in the growth period. Cell-free extracts of washed cell suspensions, prepared by hand grinding or lysozyme treatment, had no demonstrable intracellular protective antigen. Sonic treatment released antigen in measurable amounts, but tended to destroy or degrade the labile antigen. Freezing and thawing disrupted the cells and liberated the antigen; protective antigen was shown to be of internal rather than of extracellular origin. Maximal intracellular antigen concentration occurred before the peak concentration was reached in the culture filtrates. Antigen also was found in cell extracts from bicarbonate-free culture media when none was present in the corresponding culture filtrates. A high level of internal protective antigen was present in cells grown in a bicarbonate-free medium maintained at a constantly alkaline pH; only a trace of antigen was present in the corresponding pH-adjusted culture filtrate. The hypothesis is presented that bicarbonate functions to control cellular permeability and release of antigen from the cells into the ambient medium.

Anthrax↗
PubMed1989

Effect of sodium bicarbonate ingestion upon repeated sprints.

The purpose of the study was to assess the effect of sodium bicarbonate ingestion upon repeated bouts of intensive short duration exercise. Twenty-three subjects participated in the investigation (8 females and 15 males, age 21.4 +/- 2.3, mean +/- sd). Subjects completed six trials; three following the ingestion of sodium bicarbonate (300 mg/kg body weight) and three following the ingestion of a placebo (8 g sodium chloride). Each trial consisted of ten ten-second sprints on a cycle ergometer with 50 seconds recovery between each sprint. 'Peak power' and 'average power output' during each ten second sprint was measured from the flywheel of the ergometer using a light-sensitive monitor (Cranlea) linked to a BBC microcomputer. The power outputs recorded during each ten-second sprint of the bicarbonate trials were then compared with those recorded during the corresponding sprint of the placebo trials. The bicarbonate trials produced higher mean 'average power' outputs in all ten of the ten-second sprints, with the difference in 'average power' output being statistically significant in eight of these (p less than 0.05). The results also revealed that the difference in the 'average power' outputs attained during the bicarbonate and placebo trials increased as the number of sprint repetitions increased (p less than 0.01). 'Peak power' output was also greater in the bicarbonate trials with it being significantly higher (p less than 0.001) during the final ten-second sprint. It was concluded that during exercise consisting of repeated, short-duration sprints, power output was enhanced following the ingestion of sodium bicarbonate, (300 mg/kg body weight).

Adolescent↗
PubMed1988

Effect of bicarbonate on efficacy of oral rehydration therapy: studies in an experimental model of secretory diarrhoea.

In situ perfusion of rat intestine was used to evaluate the effect of bicarbonate on the efficacy of a low sodium (35 mmol/l) glucose-electrolyte oral rehydration solution in normal and cholera toxin-treated rat small intestine. In normal intestine, absorption of water was greater (108 (8.1) microliters/min/g; p less than 0.01) and sodium secretion less (-4.3 (0.3) mumol/min/g; p less than 0.01) from the oral rehydration solution containing bicarbonate than from the solution in which bicarbonate was replaced by chloride ions (59.5 (7.2) microliters/min/g and -7.8 (0.8) mumol/min/g, respectively). Glucose absorption in normal intestine was similar with both solutions. In the secreting intestine, both oral rehydration solutions reversed net water secretion to absorption, but inclusion of bicarbonate resulted in significantly less net absorption of both water (2.18 (6.9) microliters/min/g; p less than 0.05) and glucose (18.7 (2.1) mumol/min/g; p less than 0.001) compared with bicarbonate free oral rehydration solution (19.4 (3.9) microliters/min/g and 35.8 (3.7) mumol/min/g, respectively). Net sodium secretion occurred in normal and secreting intestine but was significantly less with the bicarbonate containing oral rehydration solution. These findings suggest that the demonstrable advantage of bicarbonate in promoting water absorption from this oral rehydration solution in normal rat intestine does not apply to cholera toxin treated secreting intestine.

Animals↗
PubMed1995

Muscarinic M1 receptor inhibition reduces gastroduodenal bicarbonate secretion and promotes gastric prostaglandin E2 synthesis in healthy volunteers.

The selective muscarinic M1 receptor antagonist, pirenzepine, considerably stimulates duodenal mucosal bicarbonate secretion in the rat and increases gastric luminal release of prostaglandin E2 (PGE2) in humans. This study, therefore, looked at the effect of pirenzepine on bicarbonate secretion and luminal output of PGE2 into the stomach and the duodenum of nine healthy volunteers using a new technique permitting simultaneous measurements. In the stomach modified sham feeding increased bicarbonate secretion from 382 (62) mumol/h (mean (SEM)) to 959 (224) mumol/h (p < 0.02). In the duodenum modified sham feeding and acid exposure (HCl 0.1 M; 20 ml; 5 min) of the duodenal bulb increased mucosal bicarbonate secretion from 191 (14) mumol/cm x h to 266 (27) mumol/cm x h (p < 0.02) and 634 (157) mumol/cm x h (p < 0.01), respectively. Pirenzepine (10 mg/h intravenously) reduced basal and vagally stimulated gastric and basal duodenal bicarbonate secretion by about 50% (p < 0.03). In the stomach, but not the duodenum, basal and vagally stimulated PGE2 output increased significantly (p < 0.05) in response to pirenzepine. In conclusion, human gastroduodenal mucosal bicarbonate secretion is regulated by a pirenzepine sensitive mechanism, which is probably cholinergic. The rise in gastric PGE2 output seen in response to M1 receptor inhibition by pirenzepine suggests the existence of a feed back loop secondary to the decrease seen in bicarbonate secretion.

Adult↗
PubMed1996

Omeprazole promotes proximal duodenal mucosal bicarbonate secretion in humans.

The proton pump inhibitor, omeprazole, surprisingly resulted in higher rates of proximal duodenal mucosal bicarbonate secretion than previously reported using an H2 receptor antagonist for gastric acid inhibition. Gastroduodenal perfusions were performed in healthy volunteers to evaluate whether this incidental finding is explained by more potent gastric acid inhibition by omeprazole or might be caused by the different mode of drug action. Basal and stimulated gastric and duodenal bicarbonate secretion rates were measured in the same subjects in control experiments (n = 17) and after pretreatment with high dose omeprazole (n = 17) and ranitidine (n = 9), respectively, by use of a technique permitting simultaneous measurements. Concentrations of bicarbonate were measured in the respective effluents by the method of back titration. Both omeprazole and ranitidine completely inhibited gastric acid secretion (pH 6.9 v 6.8; p > 0.05). Omeprazole caused higher rates of basal (mean (SEM)) (597 (48) v 351 (39) mumol/h; p < 0.02) and vagally stimulated (834 (72) v 474 (66) mumol/h; p < 0.02), but not acid stimulated (3351 (678) v 2550 (456) mumol/h; p > 0.05) duodenal bicarbonate secretion compared with control experiments. Also the combination of omeprazole and ranitidine increased (p = 0.05) duodenal bicarbonate secretion, while ranitidine alone caused no change in either basal or stimulated secretion. In the stomach basal as well as vagally stimulated bicarbonate secretion was independent of the means of acid inhibition. These results show that the proton pump inhibitor, omeprazole, promotes proximal duodenal mucosal bicarbonate secretion apparently independent of its gastric acid inhibitory effect. The mechanism of action remains speculative.

Adult↗
PubMed1989

Effect of VIP antagonist on VIP-, PGE2-, and acid-stimulated duodenal bicarbonate secretion.

Vasoactive intestinal peptide (VIP), prostaglandin E2 (PGE2), and luminal acidification are each potent stimulants of duodenal mucosal bicarbonate secretion. The present experiments were performed to determine whether the recently described VIP antagonist, [4Cl-D-Phe6,Leu17]VIP, suppresses VIP-stimulated duodenal mucosal bicarbonate secretion and to determine whether VIP serves as a mediator of bicarbonate secretion stimulated by acid or PGE2. In anesthetized rats, the effects of intravenous VIP, intraluminal PGE2, and intraluminal HCl on duodenal mucosal bicarbonate secretion both in the presence and absence of [4Cl-D-Phe6,Leu17]VIP were measured. The VIP antagonist inhibited duodenal bicarbonate secretion stimulated by both intravenous VIP and luminal acidification but not luminal PGE2. These findings suggest that VIP could be one mediator of acid-induced duodenal bicarbonate secretion and that the mechanism of PGE2-stimulated bicarbonate secretion is independent of VIP.

Animals↗
PubMed1990

Intrahypothalamic corticotropin-releasing factor elevates gastric bicarbonate and inhibits stress ulcers in rats.

The effects of intrahyopthalamic microinfusions of corticotropin-releasing factor (CRF) on gastric bicarbonate, acid, and pepsin content and on cold restraint-induced gastric lesion formation were tested in three experiments. Bilateral microinfusions of CRF into the hypothalamic ventromedial nucleus (0.86 nmol/rat) significantly increased both gastric bicarbonate concentration and total bicarbonate output. These effects were observed irrespective of whether rats were pretreated with the acid antisecretory drug omeprazole. In nonomeprazole-pretreated rats, CRF microinfusions also significantly reduced acid secretion and raised pH. The increase in bicarbonate content accounted for half of the observed decrease in acid output, suggesting that CRF microinfusions activated separable bicarbonate-stimulating and acid-inhibiting hypothalamic systems. In non-omeprazole-pretreated rats, CRF microinfusions significantly increased serum gastrin, whereas pepsin output was unchanged. Gastric mucosal damage produced by 4 h of cold restraint was significantly diminished by CRF microinfusion into the ventromedial hypothalamus. These data demonstrate that ventromedial hypothalamic microinfusions of CRF increase bicarbonate content, decrease gastric acid content, and confer protection against cold restraint-induced gastric mucosal damage. Hypothalamic CRF neuronal terminals and receptors may be involved in the central regulation of gastric bicarbonate secretion as well as acid secretion.

Animals↗
PubMed1976

Intracellular bicarbonate of skeletal muscle under different metabolic states.

Intracellular bicarbonate of single muscle fibers in vivo was measured by a direct electrometric method simultaneously with the membrane PD in rats under seven different metabolic states. From the measured intracellular bicarbonate values and the PCO2, the bicarbonate equilibrium potential and the intracellular pH were calculated. The mean intracellular [HCO3-] under normal control conditions was 10.3 +/- 0.7 mM (SE). The intracellular bicarbonate fell significantly in both chronic metabolic acidosis and chronic K+ depletion. In contrast, intracellular bicarbonate was elevated in chronic metabolic alkalosis, K+ loading, and Na+ depletion. Taking intracellular pH as an index of the acid-base status of cells, we find that whereas the calculated cell pH decreased along with the cell bicarbonate in both chronic metabolic acidosis and K+ depletion, cell pH increased along with the bicarbonate only in chronic metabolic alkalosis. Cell pH was unchanged in both chronic K+ loading and Na+ depletion.

Acid-Base Equilibrium↗
PubMed1981

Acid excretion by bicarbonate-free perfused rat kidney.

We measured titratable acid (TA) and NH4 excretion by isolated rat kidneys perfused either with conventional bicarbonate-containing solutions or with solutions in which bicarbonate was replaced by propionate. Rates of TA excretion by bicarbonate-perfused kidneys were similar to in vivo values, 0.27 +/- 0.04 mueq.ml GF-1 (0.21 mueq.min-1.g-1), and increased significantly under bicarbonate-free conditions to 0.70 +/- 0.12 mueq.ml GF-1 (0.42 mueq.min-1.g-1). At the same time the perfusate/urine pH difference (delta pH) increased significantly, from 0.63 +/- 0.06 to 0.92 +/- 0.06. Carbonic anhydrase inhibition by 5 X 10(-4) M acetazolamide alkalinized the urine of bicarbonate-perfused kidneys, while in the bicarbonate-free preparation the urine remained acid (delta pH = 0.27 +/- 0.04) and titratable acid continued to be excreted, though at a reduced rate, 0.19 +/- 0.04 mueq.ml GF-1. Under these same bicarbonate-free carbonic anhydrase-inhibited conditions, lowering the perfusate pH from 7.4 to 7.1 increased delta pH to 0.36 +/- 0.02 and caused total acid excretion (TA + NH4) to rise from 0.29 +/- 0.04 to 0.45 +/- 0.06 mueq.ml GF-1, and increasing the perfusate [HPO4] from 2.4 to 9.6 mM increased TA to 0.80 +/- 0.09 mueq.ml GF-1.

Acetazolamide↗
PubMed1981

Tubular handling of bicarbonate and chloride in the dog.

Bicarbonate reabsorption was assessed in the superficial proximal and distal tubule of the hydropenic dog. Tubule fluid bicarbonate concentration was measured by determination of total CO2 with microcalorimetry. Total CO2 declined from 21 to 14 mM along the proximal tubule, which reabsorbed 56% of the filtered bicarbonate prior to the late proximal sampling site. Absolute bicarbonate reabsorption was 124 pmol . min-1 . mm tubule length-1. Concurrent water reabsorption was 34% of the glomerular filtration rate. Tubule fluid-to-ultrafilterable chloride concentration ratio rose to 1.10 as the tubule fluid-to-blood bicarbonate ratio fell to 0.69 at the late proximal collection site. The total CO2 in distal tubule fluid was 6 mM, indicating that 94% of the filtered bicarbonate was reabsorbed prior to the distal tubule. It is concluded that bicarbonate is reabsorbed in preference to chloride in the superficial proximal tubule of the dog, which, like that of the rat, may provide a potential driving force for water and salt reabsorption.

Animals↗