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PubMed1998

Molecular cloning of a new sodium bicarbonate cotransporter cDNA from human retina.

Sodium bicarbonate cotransport is an electrogenic process and a principal regulator of pH. A recently cloned sodium bicarbonate cotransporter (NBC1) is predominantly expressed in kidney. The presence of several isoforms is suggested from functional studies. We have cloned a new member of this family from human retina, which was named hNBC2 (for human sodium bicarbonate cotransporter 2). The hNBC2 has 1018 amino acid residues with 10 hydrophobic transmembrane domains. A cluster of five N-glycosylation sites is present at the second extracellular loop. It has 53% amino acids identity with hNBC1 and 38% identity with anion exchanger 1. Thus, NBC2 is a new member of the anion exchanger superfamily. Northern blot of human tissues revealed its expression in many tissues such as testis, spleen, ovary, small intestine, colon, thymus, heart, and muscle (8.5 kb). The predominant expression at retina was documented with Northern blot of rat tissues. NBC2 may be a major regulator of extracellular pH of retina where light stimulation produces an extracellular alkalization and may contribute as a solute transporter to the prevention of retinal detachment.

Amino Acid Sequence↗
PubMed1999

Possible involvement of a chloride-bicarbonate exchanger in apoptosis of endothelial cells and cardiomyocytes.

We examined the role of ion movement in staurosporine-induced apoptosis of vascular endothelial cells. Cultured vascular endothelial cells from bovine carotid arteries were used. Apoptosis was determined by propidium iodide assay. Treatment of the endothelial cells with staurosporine (10 nmol/l-1 micromol/l) for 6 h induced nuclear fragmentation in a dose-dependent manner. Staurosporine (1 micromol/l) elicited apoptosis in 70.5+/-1.5% of cells. Concomitant treatment of endothelial cells with 1 mmol/l of 4, 4-diisothiocyanatostilbene-2,2-disulfonic acid (DIDS), a chloride-bicarbonate exchange blocker, completely inhibited staurosporine-induced apoptosis. Other ion transporter inhibitors such as dimethyl amiloride and anthracene-9 carboxylic acid were less effective inhibitors of staurosporine-induced apoptosis of endothelial cells. DIDS prevented staurosporine-induced apoptosis of endothelial cells as well as cardiomyocytes. Next, we determined whether chloride ions or bicarbonate are involved in apoptosis. Incubation with a chloride ion removal buffer did not inhibit staurosporine-induced apoptosis of endothelial cells. However, endothelial cell apoptosis was completely suppressed by an inhibitor of caspase, benzyloxycarbonyl-Asp-CH(2)-O(C)O-dichlorobenzene (zD-dcb, 50 micromol/l). Staurosporine (1 micromol/l) increased the intracellular pH of endothelial cells, and DIDS (1 mmol/l), but not a caspase inhibitor, inhibited this increase in pH caused by staurosporine. Our findings suggest that endothelial cell apoptosis induced by staurosporine may be associated with the Cl(-)and bicarbonate (HCO-3) ions. Thus, Cl(-)efflux from cells or HCO-3 influx to cells (which increases pH) may play an important role in signal transduction leading events such as activation of caspase in staurosporine-induced apoptosis.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1985

Electrical properties of Madin-Darby canine kidney cells. Effects of extracellular potassium and bicarbonate.

To gain some insight into electrogenic transport processes across the plasma membrane of Madin-Darby canine kidney (MDCK)-cells, continuous measurements of the potential difference across the plasma measurements of the potential difference across the plasma membrane (PD) were made during step changes of extracellular ion composition as well as application of barium or valinomycin. During control conditions mimicking in vivo extracellular fluid, PD approaches -51.5 +/- 0.8 mV (n = 62). Step increase of extracellular potassium concentration from 5.4 to 10, to 20 or to 35 mmol/l, depolarizes PD by +5.5 +/- 0.8 mV (n = 7), by +15.8 +/- 0.5 mV (n = 64) and by +23.8 +/- 1.2 mV (n = 12), respectively. 1 mmol/l barium depolarizes PD by +19.8 +/- 0.6 mV (n = 38) and abolishes the effect of increasing extracellular potassium from 5.4 to 10 mmol/l but not to 35 mmol/l. Ten mumol/l valinomycin hyperpolarizes PD to -69.3 +/- 2.9 mV (n = 7). In the presence of valinomycin, increase of extracellular potassium from 5.4 to 20 mmol/l depolarizes PD by +31.0 +/- 1.0 mV (n = 7). Ouabain depolarizes PD and reduces the sensitivity of PD to extracellular potassium concentration. Omission of extracellular bicarbonate and carbon dioxide as well as increase of extracellular bicarbonate at constant carbon dioxide lead to a hyperpolarization and enhanced sensitivity of PD to extracellular potassium. In the presence of barium, the effects of omitted bicarbonate and carbon dioxide of MDCK-cells is highly conductive to potassium.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Effect of acute sodium bicarbonate ingestion on excess CO2 output during incremental exercise.

The effect of bicarbonate ingestion on total excess volume of CO2 output (CO2 excess), due to bicarbonate buffering of lactic acid in exercise, was studied in eight healthy male volunteers during incremental exercise on a cycle ergometer performed after ingestion (0.3 g.kg-1 body mass) of CaCO3 (control) and NaHCO3 (alkalosis). The resting arterialized venous blood pH (P < 0.05) and bicarbonate concentration ([HCO3-]b; P < 0.01) were significantly higher in acute metabolic alkalosis [AMA; pH, 7.44 (SD 0.03); [HCO3-]b, 29.4 (SD 1.5) mmol.l-1] than in the control [pH, 7.39 (SD 0.03); [HCO3-]b, 25.5 (SD 1.0) mmol.l-1]. The blood lactate concentrations ([la-]b) during exercise below the anaerobic threshold (AT) were not affected by AMA, while significantly higher [la-]b at exhaustion [12.29 (SD 1.87) vs 9.57 (SD 2.14) mmol.l-1, P < 0.05] and at 3 min after exercise [14.41 (SD 1.75) vs 12.26 (SD 1.40) mmol.l-1, P < 0.05] were found in AMA compared with the control. The CO2 excess increased significantly from the control [3177 (SD 506) ml] to AMA [3897 (SD 381) ml; P < 0.05]. The CO2 excess per body mass was found to be significantly correlated with both the increase of [la-]b from rest to 3 min after exercise (delta[la-]b; r = 0.926, P < 0.001) and with the decrease of [HCO3-]b from rest to 3 min after exercise (delta [HCO3-]b; r = 0.872, P < 0.001), indicating that CO2 excess per body mass increased linearly with both delta [la-]b and delta [HCO3-]b.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Sodium bicarbonate ingestion improves performance in interval swimming.

In an effort to determine the effects of bicarbonate (NaHCO3) ingestion on exercise performance, ten male college swimmers were studied during five different trials. Each trial consisted of five 91.4 m (100-yd) front crawl swims with a two-minute rest interval between each bout. The trials consisted of two NaHCO3 treatments, two placebo trials and one test with no-drink. One hour before the onset of swimming, the subjects were given 300 ml of citric acid flavored solution containing either 17 mmol of NaCl (placebo) or 2.9 mmol of NaHCO3.kg-1 body weight (experimental), or received no drink (no-drink). Performance times for each 91.4 m swim were recorded. Blood samples were obtained before and one hr after treatment, two min after warmup, and two min after the final 91.4 m sprint. Blood pH, lactate, standard bicarbonate (SBC) and base excess (BE) were measured. No differences were found for performance or the blood measurements between the placebo and no-drink trials. Bicarbonate feedings, on the other hand, produced a significant (P less than 0.05) improvement in performance on the fourth and fifth swimming sprints. Blood lactate, pH, SBC and BE were significantly higher (P less than 0.05) at post-exercise in NaHCO3 treatments. These data are in agreement with previous findings that during repeated bouts of exercise pre-exercise administration of NaHCO3 improves performance, possibly by facilitating the efflux of hydrogen ions from working muscles and thereby delaying the onset of fatigue.

Bicarbonates↗
PubMed1990

Bicarbonate stimulation of Na+ transport in liver basolateral plasma membrane vesicles requires the presence of a transmembrane pH gradient.

The effect of bicarbonate on the uptake of 22Na+ into liver basolateral plasma membrane vesicles was studied under conditions where the pH of the medium was controlled by the use of high buffer concentrations. Bicarbonate stimulated the rate of Na+ uptake only in the presence of a pH gradient (acid inside). The stimulation by bicarbonate was inhibited by both amiloride and DIDS. No evidence for electrogenic Na+/HCO3- symport was found. These results are in part consistent with electroneutral Na+/HCO3- symport, but other explanations cannot be excluded.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1989

Effects of sodium bicarbonate on nitrogen metabolism and ketone bodies during very low energy protein diets in obese subjects.

This study evaluated the effects of oral sodium bicarbonate (NaHCO3) supplementation on ammonium (NH4+) nitrogen (N) and urea N excretion and on ketone bodies during the metabolic acidosis of a very low energy protein diet. Ten healthy obese female subjects (BMI, 38.4 +/- 1.5 kg/m2;weight, 100 +/- 4 kg) were given a 1.72 MJ (412 kcal) all protein (16.8 g N) liquid formula, 16 mmol KCl and a multivitamin-mineral supplement daily for 4 weeks. In addition, the five subjects in group 1 received 60 mmol Na+ daily as sodium chloride (NaCl) for 3 weeks and as NaHCO3 during week 4. The subjects in group 2 were given 40 mmol/d NaHCO3 during the first week, 60 mmol/d during weeks 2 and 3, and 60 mmol/d NaCl during week 4. Nitrogen balance was achieved in both groups by the end of week 3. The subjects in group 1 at week 2 showed an increase in blood [H+] of 0.41 +/- 0.06 x 10(-8) mol/L and a decrease in blood bicarbonate from 26.0 +/- 0.8 to 23.8 +/- 1.2 mmol/L. The subsequent NaHCO3 curtailed NH4+ N excretion by one half, without significant change in ketone body levels or excretion. Administration of NaHCO3 from the start of the diet to the subjects in group 2 prevented both the metabolic acidosis and the increase in NH4+ N excretion and attenuated the increase in blood and urine 3-hydroxybutyrate. When NaCl replaced NaHCO3 during week 4, ammonium N excretion doubled. Urea N excretion was comparable in both groups and was unaffected by bicarbonate.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Bicarbonate in the treatment of metabolic acidosis: effects on hepatic intracellular pH, gluconeogenesis, and lactate disposal in rats.

The effects of agents used in the treatment of metabolic acidosis could depend on the induced changes in intracellular pH (pHi). To determine the effect of sodium bicarbonate on hepatic pHi and function, this agent was infused into anesthetized rats with acute metabolic acidosis due to either diabetic ketoacidosis (DKA) or HCl infusion. Hepatic pHi was measured by 31P-magnetic resonance spectroscopy (MRS). A substantial increase in pHi occurred (from 7.13 +/- 0.08 to 7.32 +/- 0.08, P < .05) despite an increase in mixed venous PCO2. Isolated livers from normal rats or those with DKA were perfused at pH 6.8 and normal PCO2. With infusion of sodium bicarbonate, there was again an increase in pHi (delta pHi, + 0.27 +/- 0.06, P < .02) despite increases in both portal and hepatic venous PCO2. Lactate uptake was increased twofold to threefold (P < .001) by bicarbonate infusion in perfusions from both types of animals. Glucose output was increased twofold (P < .001) only in livers from normal animals.

Acidosis↗
PubMed1988

The effects of intravenous theophylline infusion versus intravenous sodium bicarbonate infusion on lithium clearance in normal subjects.

Ten normal subjects ingested lithium carbonate (600 mg p.o. b.i.d.) for three 1-week intervals. At the end of each weekly interval, subjects' lithium clearances were randomly perturbed for 12 hours with the subject in a supine position by infusing either normal saline (308 mEq), sodium bicarbonate (350 mEq) in normal saline (308 mEq), or theophylline (mean = 14.0 micrograms/ml) in normal saline (308 mEq). Subjects were placed on a 200 mEq/day sodium diet during the lithium clearance perturbation stages of the study. When each patient's normal saline lithium clearance was used as a control, it was found that the theophylline produced a significantly greater % increase in lithium clearance than did the sodium bicarbonate. Theophylline infusions increased patients' individual lithium clearances by 51 +/- 52%, while sodium bicarbonate infusions increased lithium clearances by 0.6 +/- 33%. Theophylline infusions ought to be investigated as an alternative to hemodialysis in lithium intoxications requiring the immediate reduction of lithium concentrations.

Adult↗
PubMed1999

Assessment of biliary bicarbonate secretion in humans by positron emission tomography.

BACKGROUND & AIMS: Positron emission tomography (PET) allows imaging and quantitative analysis of organ functions in basal and stimulated conditions. We have applied this method to the study of biliary bicarbonate secretion in humans. METHODS: PET was performed in 5 healthy subjects and 13 patients with hepatobiliary disorders after intravenous injection of NaH11CO3. In each case the study was performed in basal conditions and after secretin stimulation. Positron emission from the hepatic area was scanned, and normalized uptake values for parenchymal and hilar regions were estimated. RESULTS: In healthy individuals, the injection of NaH11CO3 resulted in a peak uptake of the label in parenchymal and hilar regions 2-3 minutes after the injection. In both normal and cirrhotic subjects, secretin administration increased bicarbonate uptake in the parenchymal region, followed by accumulation of the label in the perihilar area. Normal basal uptake with absent response to secretin was registered in extrahepatic biliary obstruction and in untreated primary biliary cirrhosis (PBC). The secretin response was present in patients with PBC undergoing treatment with ursodeoxycholic acid. CONCLUSIONS: PET allows investigation of biliary bicarbonate secretion in humans. An impaired response to secretin was observed in cholestatic conditions. Preliminary data suggest that ursodeoxycholic acid might improve the response to secretin in PBC.

Adult↗
PubMed1986

Bicarbonate versus citrate in oral rehydration therapy in infants with watery diarrhea: a controlled clinical trial.

In a double-blind, randomized trial, we compared the efficacy of bicarbonate-containing oral rehydration solution vs citrate-containing solution in the treatment of infantile diarrheal dehydration and acidosis. Ninety-seven infants 3 to 24 months of age were entered in the study; 49 received bicarbonate-containing solution and 48 citrate-containing solution. The two groups were similar in all respects at the beginning of the study. Oral rehydration was successful (i.e., no intravenously administered fluids were required) in 85% of study patients; the success rate was similar in both treatment groups. Serum total CO2 concentration increased in a similar fashion in both groups, reaching near normal values at 48 hours after admission. We conclude that sodium citrate can be substituted for sodium bicarbonate in the formulation of the orally administered rehydration solution recommended by the World Health Organization for treatment of diarrheal dehydration in infants.

Bicarbonates↗
PubMed1984

Effects of acidemia and sodium bicarbonate therapy in advanced cardiac life support.

Cardiac output using the currently recommended closed-chest cardiopulmonary resuscitation (CPR) technique is marginal (less than 30% of control), and eventually will result in tissue hypoperfusion and lactic acidemia. Intermittent sodium bicarbonate administration currently is recommended for treatment of this metabolic acidemia, and based on available data recommended dosages are empiric but sound. In this review the potential complications of acidemia and sodium bicarbonate administration are considered from the viewpoint of resuscitation outcome. In our opinion, available data are limited, and further evaluation and consideration of sodium bicarbonate requirements in the resuscitation setting are required.

Acidosis, Respiratory↗
PubMed1987

Acetate dialysate versus bicarbonate dialysate: a continuing controversy.

The use of bicarbonate dialysate as the buffer during routine dialysis is growing. This discussion reviews several of the comparative trials in which bicarbonate and acetate buffers have been tested. Effects of the two buffers on BP, cardiac function, and pulmonary performance are discussed. Costs of the two systems are also compared. Patients who seem most likely to benefit from bicarbonate dialysate include those with a reduced muscle mass in whom a high sodium dialysate has not prevented hypotension.

Acetates↗
PubMed1991

Bioavailability of erythromycin acistrate from hard gelatin capsules containing sodium bicarbonate.

Erythromycin acistrate is a new prodrug of erythromycin. Its bioavailability from hard gelatin capsules containing the drug with or without sodium bicarbonate was studied in healthy volunteers. The plasma levels of erythromycin, anhydroerythromycin, and acetylerythromycin were measured using an HPLC method. Addition of sodium bicarbonate to the capsule markedly enhanced the plasma level of the microbiologically active substance, erythromycin, doubling the Cmax and AUC values (P less than 0.05). At the same time, the lag time in the absorption curve was shortened to one-third. No changes in the plasma levels of the inactive metabolite anhydroerythromycin were noted. It is concluded that adding sodium bicarbonate to an erythromycin acistrate formulation enhances its bioavailability.

Adult↗
PubMed1987

Sodium-bicarbonate cotransport occurs in rat kidney cortical membranes but not in rat small intestinal basolateral membranes.

Basolateral membrane vesicles were isolated from rat kidney cortex and small intestinal enterocytes. Both membrane preparations show ATP-dependent calcium uptake and cytochalasin B-sensitive D-glucose transport. In renal membranes, sodium influx is stimulated by bicarbonate; bicarbonate-dependent sodium flux is membrane-potential-dependent and inhibited by 4,4'-di-isothiocyanato-2, 2'-stilbenedisulphanic acid ('DIDS'). Small intestinal basolateral membranes do not show bicarbonate-dependent sodium fluxes.

Adenosine Triphosphate↗
PubMed1998

Permeability defect with bicarbonate leak as a mechanism of immune-related distal renal tubular acidosis.

We present a 15-year-old girl with distal renal tubular acidosis (dRTA) appearing in what is probably a very early stage of primary Sjögren's syndrome. On the basis of tests evaluating renal handling of H+, we attempt to explain the mechanism of the urine acidification disorder. The inability to decrease urinary pH during systemic acidosis, together with the normal increase of urinary carbon dioxide partial pressure (pCO2) values after sodium bicarbonate and neutral phosphate loading, suggest a gradient-type dRTA. The inability to lower urinary pH in response to furosemide, accompanied by markedly increased urinary excretion of NH4, HCO3, Na, and K, points to a collecting tubule permeability disorder with bicarbonate leak to the tubular lumen. This patient had never been exposed to amphotericin B. To our knowledge, immune-related dRTA as a result of a gradient defect with bicarbonate leak into the tubular lumen has not been described.

Acidosis, Renal Tubular↗
PubMed1983

Effect of sodium bicarbonate pretreatment on barium coating of mucosa during double contrast barium meal.

The radiographic pattern of the areae gastricae is produced by barium lying in the intersecting furrows of the gastric mucosal surface. However, if the mucus layer on the gastric mucosa is thick, it interferes with the barium coating of the areae gastricae during double contrast barium meal. As sodium bicarbonate decreases the viscosity of mucus and thus may make the gastric mucus layer thinner, it was evaluated as a pretreatment agent in a routine double contrast upper-gastrointestinal study to improve the visualization of the areae gastricae. In a single blind study, 53 of 106 patients took sodium bicarbonate water mixtures at bedtime the day before and on the morning of the examination. According to the results of the present study mucolysis induced by the used doses of sodium bicarbonate does not significantly affect micromucosal visualization during double-contrast barium meal.

Adult↗
PubMed1992

Bicarbonate ingestion: effects of dosage on 60 s cycle ergometry.

Nine healthy male subjects who were all participating in athletic events volunteered to take part in this study, the aim of which was to determine whether there are specific dosages of sodium bicarbonate (HCO3-) that are useful as an ergogenic aid as far as anaerobic performance times are concerned. A control, placebo (CaCO3 500 mg kg-1) and five dosages of bicarbonate (100, 200, 300, 400 and 500 mg kg-1) were used. The anaerobic test consisted of pedalling a Repco Exertech cycle ergometer for 1 min during which total work (kJ) and peak power (W) were measured. The subjects completed more work in the 200 (P < 0.05), 300, 400 and 500 mg kg-1 (P < 0.005) trials with most work being undertaken in the 300 mg kg-1 trial (41.9 kJ min-1). Peak power was not significantly different from the control until the 300 mg kg-1 dose, and there were no further changes from this with increasing doses of HCO3-. The highest level of peak power achieved was 1295 +/- 72.8 W at the 300 mg kg-1 dosage. Blood pH indicated that after ingestion of all but the 100 mg kg-1 dose, a state of alkalosis was achieved (P < 0.005), and this was also indicated by changes in base excess. Bicarbonate levels increased post-ingestion in all but the 100 mg kg-1 dose, with these changes reflecting the changes that occurred in the work output. Blood lactate (BLa) levels increased post-exercise (P < 0.0001).(ABSTRACT TRUNCATED AT 250 WORDS)

Acid-Base Equilibrium↗