SEARCH · Search PubMed

Results for “Bicarbonates”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

SourceResearch connectionFrom yearThrough year

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 181 records · Page 10Linked to original sources

PubMed1986

Acid-base regulation and ion transfers in the carp (Cyprinus carpio): pH compensation during graded long- and short-term environmental hypercapnia, and the effect of bicarbonate infusion.

To study both temporal and quantitative effects of hypercapnia on the extent of pH compensation in the arterial blood, specimens of carp (Cyprinus carpio) were exposed to a PCO2 of about 7.5 mmHg (1 mmHg = 133.3 Pa) (1% CO2) in the environmental water for several weeks, and a second group of animals was subjected to an environmental PCO2 of about 37 mmHg (5% CO2) for up to 96 h. A third series of experiments was designed to test the possibility that infusion of bicarbonate would increase the extent of plasma pH compensation. Dorsal aortic plasma pH, PCO2 and [HCO3-], as well as net transfer of HCO3- -equivalent ions, NH4+, Cl- and Na+, between fish and ambient water, were monitored throughout the experiments. Exposure to environmental PCO2 of 7.5 mmHg resulted in the expected respiratory acidosis with the associated drop in plasma pH, and subsequent compensatory plasma [HCO3-] increase. The compensatory increase of plasma bicarbonate during long-term hypercapnia continued during 19 days of exposure with plasma bicarbonate finally elevated from 13.0 mmoll-1 during control conditions to 25.9 mmoll-1 in hypercapnia, an increase equivalent to 80% plasma pH compensation. Exposure to 5% hypercapnia elicited much larger acid-base effects, which were compensated to a much lesser extent. Plasma pH recovered to only about 45% of the pH depression expected at constant bicarbonate concentration. At the end of the 96-h exposure period, plasma [HCO3-] was elevated by a factor of 2.5 to about 28.2 mmoll-1. The observed increase in plasma bicarbonate concentration during 5% hypercapnic exposure was attributable to net gain of bicarbonate equivalent ions from (or release of H+-equivalent ions to) the environmental water. Quantitatively, the gain of 15.6 mmol kg-1 was considerably larger than the amount required for compensation of the extracellular space, suggesting that acid-base relevant ions were transferred for compensation of the intracellular body compartments. The uptake of bicarbonate-equivalent ions from the water was accompanied by a net release of Cl-and, to a smaller extent, by a net uptake of Na+, suggesting a 75% contribution of the Cl-/HCO-3 exchange mechanism. Infusion of bicarbonate after 48 h of exposure to 7.5 mmHg PCo2 had only a transient effect on further pH compensation. The infused bicarbonate was lost to the ambient water, and pre-infusion levels of bicarbonate were reattained within 24 h. Repetition of the infusion did not result in a notable improvement of the acid-base status.(ABSTRACT TRUNCATED AT 400 WORDS)

Acid-Base Equilibrium↗

PubMed1986

Effect of depletion of phosphate and bicarbonate ions on insulin action in rat adipocytes.

The effect of insulin on rat adipocytes was studied in isotonic buffers (pH 7.4) containing NaCl, CaCl2, MgSO4, KCl, and bovine serum albumin but no phosphate or bicarbonate anions. In phosphate- and bicarbonate-free buffers the dose-response curve to insulin is shifted to the right, the effects of the hormone on hexose uptake, glucose metabolism, and inhibition of lipolysis being observed at much higher (nearly 2 orders of magnitude) concentrations of insulin. The insulin binding capacity of the cells is only slightly changed. The dose-response curve for isoproterenol which stimulates lipolysis in the same cell type is almost the same in both Krebs-Ringer bicarbonate buffer and phosphate- and bicarbonate-free buffers. The dose-response curves for agents that mimic the action of insulin such as wheat germ agglutinin or vanadate ions are also shifted to the right. The dose-response curve to insulin can be returned to "normal" by readdition of either bicarbonate or phosphate. Almost complete recovery is obtained at either 10 mM bicarbonate or 24 mM phosphate, respectively. External Ca2+ ions which are not required for the proper action of insulin in fat cells maintained in Krebs-Ringer bicarbonate buffer, become essential for insulin action in bicarbonate-free buffer. The study indicates that depletion of bicarbonate and, to a lesser extent, phosphate anions, interferes with an essential insulin-dependent post-binding event. Also, in bicarbonate-free medium, external Ca2+ ions are essential for insulin-mediated processes. The implications of this study to the mode of action of insulin, and to physiological and clinical states of insulin desensitization are discussed.

3-O-Methylglucose↗

PubMed1988

Prescribing dialysate bicarbonate concentrations for hemodialysis patients.

A rearranged equation of Sargent and Gotch (1) was used to determine dialysate bicarbonate concentrations for hemodialysis patients. Parameters in this equation include an estimate of the acid generated by each patient between treatments, an estimate for the dialyzer dialysance for bicarbonate, ultrafiltration rate, blood flow rate and a targeted mid-dialysis plasma bicarbonate concentration of 25 mEq/L. Nine patients were studied over a 35 week period to verify this method of determining each patient's dialysate bicarbonate concentration. Prescribed dialysate bicarbonate concentrations for the nine patients varied from 29 to 38 mEq/L with five patients having a prescribed value of 35 mEq/L. After a baseline period of five weeks, five patients switched from a 37 mEq/L acetate dialysate to their prescribed dialysate bicarbonate concentration. Four patients who had already been on bicarbonate dialysis at a concentration of 35 mEq/L were dialyzed with their prescribed dialysate bicarbonate concentrations. Patients were then followed for a study period of 30 weeks. The prescribed dialysate bicarbonate concentration resulted in more normal acid/base chemistries for both groups of patients. The results also demonstrate that chronic hemodialysis patients require individualization of dialysate bicarbonate concentrations.

Acid-Base Equilibrium↗

PubMed1993

Bicarbonate induces sensitization of cyclic AMP accumulation by intact 1321N1 human astrocytoma cells.

Preincubation of 1321N1 human astrocytoma cells in medium buffered with bicarbonate induced 50 to 100% increases in subsequent stimulation of cyclic AMP accumulation by the beta adrenergic receptor agonist isoproterenol and by the direct adenylyl cyclase activator forskolin, compared to cells incubated in buffered medium without bicarbonate. This "bicarbonate-induced sensitization" of cyclic AMP accumulation occurred rapidly, was rapidly reversible and was bicarbonate concentration-dependent. Although protein kinase C activation also induces sensitization in these cells, sensitization by bicarbonate does not appear to involve protein kinase C, because neither protein kinase C down-regulation nor the kinase inhibitor staurosporine prevented sensitization. Pertussis toxin neither mimicked nor prevented the sensitization by bicarbonate, suggesting that pertussis toxin-sensitive guanine nucleotide-binding proteins are not involved. The effect of bicarbonate appears to be on synthesis of cyclic AMP rather than degradation, inasmuch as the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine did not prevent expression of sensitization and because cyclic AMP degradation rates were not altered after bicarbonate incubation. However, increased adenylyl cyclase activity was not retained in broken cell preparations from cells incubated with bicarbonate. These results suggest the occurrence of a novel mechanism through which bicarbonate exposure can regulate adenylyl cyclase activity in intact cells.

1-Methyl-3-isobutylxanthine↗

PubMedDate not supplied

Clinical experience with a 39 mmol/L bicarbonate-buffered peritoneal dialysis solution.

OBJECTIVE: To investigate the effect on the patient's acid-base status of a 39 mmol/L bicarbonate-buffered continuous ambulatory peritoneal dialysis (CAPD) solution. DESIGN: This was an open, controlled, cross-over, two-center study in 9 patients. After three months of treatment with a 34 mmol/L bicarbonate-buffered solution (t0) patients were switched to a 39 mmol/L bicarbonate-containing solution for four weeks. At the end of the study period (t4) patients were again treated with a 34 mmol/L bicarbonate-buffered CAPD solution for one month (t8). RESULTS: Mean venous plasma bicarbonate level significantly increased during the study and decreased at the baseline level during the control period (t0 = 22.94 +/- 2.54, t1 = 26.74 +/- 3.07, t2 = 28.47 +/- 2.68, t3 = 28.11 +/- 3.56, t4 = 28.71 +/- 3.27, t8 = 24.94 +/- 2.56). Arterial blood pH and plasma bicarbonate significantly increased during the study and significantly decreased at the end of the control period (pH: t0 = 7.37 +/- 0.04, t4 = 7.42 +/- 0.04, t8 = 7.37 +/- 0.06. Bicarbonate: t0 = 21.97 +/- 2.57, t4 = 25.85 +/- 2.02, t8 = 21.87 +/- 2.89). The changes in plasma bicarbonate during the study period were inversely correlated with the metabolic acid production calculated from the protein catabolic rate and with the apparent distribution space for bicarbonate (ABS) of patients. CONCLUSIONS: The 39 mmol/L bicarbonate-buffered CAPD solution improved the patient's acid-base status. Potential undesirable metabolic alkalosis could be prevented by analyzing the ABS and the metabolic acid production of patients.

Acid-Base Equilibrium↗

PubMed1988

The bicarbonate-dependence of zinc(II)-transferrin binding.

The binding of zinc(II) to human serum transferrin has been studied as a function of the solution concentration of sodium bicarbonate in 100 mM, pH 7.4 hepes buffer at 25 degrees C. The apparent molar absorptivity of the zinc-transferrin complex has been determined from the initial slopes of titration curves of delta epsilon versus the ratio of [Zn]/[Tf]. This absorptivity represents the difference between the positive absorbance of the ternary Zn-HCO3-Tf species in the sample cuvette and the negative absorbance of binary HCO3-Tf species in the reference cuvette. Higher concentrations of bicarbonate increase the degree of saturation of apo-Tf with bicarbonate and thus increase the apparent absorptivity of the zinc-Tf complex. Titrations of apo- and monoferric transferrins with bicarbonate indicate that there is little, if any, difference in the bicarbonate binding constants of the two specific transferrin binding sites. An equilibrium constant of log K = 2.49 has been used to calculate the degree of saturation of the C-terminal binding site with bicarbonate. The zinc-binding affinity of this site depends linearly on this degree of saturation. The scatter in the zinc-binding constants of the weaker N-terminal site precludes a similar analysis of the bicarbonate-dependence of binding at this site. The results strongly support the previous proposal that binding of the synergistic bicarbonate anion is responsible for the uv absorption observed upon addition of bicarbonate to apoTf.

Bicarbonates↗

PubMed1989

Bicarbonate inhibition of Saccharomyces cerevisiae and Hansenula wingei growth in apple juice.

The ability of sodium bicarbonate to inhibit growth of Saccharomyces cerevisiae and Hansenula wingei in apple juice was investigated. Sodium bicarbonate at concentrations of 0.06, 0.12, and 0.24 M was added to pasteurized apple juice that was then inoculated with 10(3) or 10(5) cfu/ml of either yeast. Growth of both yeasts was inhibited by 0.12 M sodium bicarbonate when incubation was at 4 degrees C; 0.24 M sodium bicarbonate caused a slow die off of yeast. At 18 degrees C, H. wingei became more sensitive and died in the presence of 0.12 M sodium bicarbonate, but S. cerevisiae became resistant to 0.24 M sodium bicarbonate. These results could not be attributed to bicarbonate-induced pH elevation or sodium. Potassium and ammonium bicarbonate were also inhibitory, implicating bicarbonate ion as the antimicrobial agent.

Beverages↗

PubMed1991

The effect of bicarbonate on resuscitation from cardiac arrest.

STUDY OBJECTIVES: This study attempted to determine the effect of bicarbonate administration on resuscitation in a porcine model of prolonged cardiac arrest. DESIGN: After instrumentation, 26 swine were subjected to ventricular fibrillation for 15 minutes (16 animals) or 20 minutes (ten animals) with no resuscitative efforts. INTERVENTIONS: Resuscitation attempts with open-chest cardiac massage and epinephrine were used in all animals after the arrest period. The experimental group was given sodium bicarbonate (3 mEq/kg), and the control group received 3% saline (5 mL/kg) at the initiation of cardiac massage. MEASUREMENTS: Resuscitation success, hemodynamics, and arterial and mixed venous gases were compared in the bicarbonate and hypertonic saline-treated groups. RESULTS: There was no difference in resuscitation rates between bicarbonate and nonbicarbonate-treated swine. After 15 minutes of ventricular fibrillation, six of eight bicarbonate-treated swine were resuscitated successfully compared with five of eight hypertonic saline-treated animals. None of the five bicarbonate-treated or five hypertonic saline-treated swine that underwent 20 minutes of ventricular fibrillation were resuscitated. The arterial and mixed venous pH values were significantly different in the bicarbonate-treated animals from values in the control group. There was no difference in systolic or diastolic blood pressures or myocardial perfusion pressure between the bicarbonate and hypertonic saline-treated animals. CONCLUSION: Despite correlation of arterial and venous acidemia, the use of sodium bicarbonate did not improve resuscitation from prolonged cardiac arrest.

Animals↗

PubMed1984

Effects of sodium bicarbonate and 1,25-dihydroxy-cholecalciferol on calcium and phosphorus balances in the rat.

Metabolic balance studies were undertaken to determine whether sodium bicarbonate (NaHCO3) supplements (4.5 mmol/day) altered 7-day cumulative calcium (Ca) phosphorus (P) balances in growing rats consuming either a basal diet providing 0.6% Ca and 0.3% P, or this diet plus 1,25-dihydroxycholecalciferol [40 ng 1,25(OH)2D3/day]. Feeding bicarbonate lowered urinary Ca but raised fecal Ca so that Ca balance became less positive. However, 1,25(OH)2D3 increased net absorption of Ca and P to the same degree when given to control rats and rats consuming bicarbonate. Nevertheless, bicarbonate-fed rats had lower net Ca absorption than controls, even when treated with high doses of 1,25(OH)2D3. Changes in net Ca absorption induced by bicarbonate may occur at a point in the gut distal to the duodenum since duodenal 45Ca absorption was decreased by bicarbonate feeding. The present results show that bicarbonate consumption depressed net Ca absorption in the rat. The effect appears to be independent of changes in 1,25(OH)2D3 metabolism because it is manifest in animals receiving high doses of 1,25(OH)2D3, which stimulate alimentary Ca absorption maximally, and because bicarbonate-fed rats are able to respond normally to exogenous 1,25(OH)2D3 by increasing their net absorption of Ca and P. In view of this demonstration that NaHCO3 supplements elevate fecal Ca loss in the rat, it is suggested that studies should be undertaken to determine whether bicarbonate exerts similar adverse effects on Ca balance in humans.

Absorption↗

PubMed1983

Influence of steady-state alterations in acid-base equilibrium on the fate of administered bicarbonate in the dog.

Previous workers have shown that metabolic acidosis increases the apparent space through which administered bicarbonate is distributed. This finding has been ascribed to the accompanying acidemia and to the consequent availability of a large quantity of hydrogen ion that accumulates on nonbicarbonate tissue buffers during the development of acidosis. To test this hypothesis, bicarbonate space was measured in dogs with a broad range of steady-state plasma [HCO-3] in association with alkalemia as well as with acidemia. Appropriate combinations of pH and plasma [HCO-3] were achieved by pretreating the animals to produce graded degrees of each of the four cardinal, chronic acid-base disorders. Metabolic acidosis (n = 15) was produced by prolonged HCl-feeding; metabolic alkalosis (n = 17) by diuretics and a chloride-free diet; and respiratory acidosis (n = 9) and alkalosis (n = 8) by means of an environmental chamber. Animals with normal acid-base status (n = 4) were also studied. Sodium bicarbonate (5 mmol/kg) was infused over 10 min to the unanesthetized animals; observations were carried out over 90 min. The results obtained from animals with metabolic acid-base disturbances demonstrated an inverse relationship between bicarbonate space and initial plasma pH, confirming the previous findings of others. By contrast, the results obtained in animals with respiratory acid-base disturbances demonstrated a direct relationship between bicarbonate space and initial plasma pH. The pooled data revealed that bicarbonate space is, in fact, quite independent of the initial pH but is highly correlated with the initial level of extracellular [HCO-3]; dogs with low extracellular [HCO-3] (congruent to 10 meq/liter) whether acidemic or alkalemic, have a bicarbonate space that is 25% larger than normal and some 50% larger than in dogs with high extracellular [HCO-3] (congruent to 50 meq/liter). We conclude from these results that the increased bicarbonate space in metabolic acidosis (and respiratory alkalosis) does not reflect the availability of more hydrogen ions for release during bicarbonate administration, but merely evidences the wider range of titration (delta pH) of nonbicarbonate buffers that occurs during alkali loading whenever plasma [HCO-3] is low.

Acid-Base Equilibrium↗

PubMed1992

Measurement of gastric bicarbonate secretion in the human stomach: different methods produce discordant results.

Human gastric bicarbonate secretion has been measured by back-titration, from pH and pressure of carbon dioxide (PCO2) determinations (using the Henderson-Hasselbalch formula), and from equations based on gastric juice osmolality and [H+] (osmolality-[H+] method). Since these methods show large quantitative differences in their estimations of gastric bicarbonate secretion, we examined each to define the reasons for these discrepancies and establish guidelines for future work in this area. Bicarbonate recovery from 'non-parietal' secretions (0 to 80 mM HCO3) reacting with 'pure parietal secretion' (160 mM HCl) was studied both in vitro and in the pylorus-occluded healthy human stomach during acid suppression, exogenous acidification, and pentagastrin stimulation. The pH/PCO2 method estimated HCO3- accurately under anaerobic conditions in vitro, whereas the osmolality-[H+] method (with correction factors for osmolality incorporated by us) was accurate under aerobic conditions. In the acid-suppressed stomach back-titration was significantly more accurate than the pH/PCO2 method. In the exogenously acidified and pentagastrin-stimulated stomachs the pH/PCO2 method underestimated bicarbonates, and the osmolality-[H+] method was spuriously elevated in the low range and diminished at high bicarbonate concentrations. Estimates of 'basal' bicarbonate secretion (at zero added bicarbonate) were severalfold higher by the osmolality-[H+] method (5.26 +/- 0.33 mmol/h) than by the pH/PCO2 method (1.20 +/- 0.23 mmol/h) or back-titration (0.65 +/- 0.14 mmol/h). In conclusion, gastric bicarbonate was determined most correctly by back-titration in the acid-suppressed stomach, whereas measurement of bicarbonate in the acid-secreting stomach was not accurate with any method.

Adult↗

PubMed1985

Response of dairy cows to sodium bicarbonate and limestone in early lactation.

A total of 108 dairy cows at three locations were fed a diet supplemented with sodium bicarbonate and limestone during the first 16 wk of lactation. Complete mixed diets were fed for ad libitum intake and consisted of concentrate and corn silage (60:40, dry matter). The four treatments were: 1) basal diet, 2) basal plus 1.2% sodium bicarbonate, 3) basal plus 1.4% limestone, and 4) basal plus 1.2% sodium bicarbonate plus 1.4% limestone. Dry matter intake was increased for 8 wk by sodium bicarbonate, then decreased from wk 9 to 16. Intake was decreased by limestone alone or in combination with sodium bicarbonate. Sodium bicarbonate increased milk production for 8 wk and 4% fat-corrected milk for 16 wk. Average dry matter intake, milk production, and 4% fat-corrected milk (kg/day) for the 16 wk were: 1) 20.2, 31.1, 27.3; 2) 19.8, 32.0, 28.7; 3) 18.9, 31.4, 27.9, and 4) 18.4, 29.7, 27.2 for diets 1 to 4. Ruminal pH was decreased, and volatile fatty acid concentration was increased by added sodium bicarbonate and appeared to result from increased feed intake. Digestibility of nutrients was unaffected by supplements. Sodium bicarbonate affected regulation of blood and urine pH and concentration of electrolytes more than limestone. Serum magnesium was reduced with sodium bicarbonate, although not beyond normal physiological reference range.

Animals↗

PubMed1984

Gas production after reaction of sodium bicarbonate and hydrochloric acid.

Ingestion of sodium bicarbonate has been implicated as one of the proximate causes of spontaneous gastric rupture. However, the volume and rate of gas released from the reaction of ingested sodium bicarbonate and gastric acid has not been previously studied in detail. We, therefore, developed an in vitro method for measuring gas release after addition of sodium bicarbonate to a solution containing hydrochloric acid. From the results of our studies, we conclude that even though hydrochloric acid and sodium bicarbonate react instantaneously, the resulting gas production is slow, mainly because CO2 produced from the dehydration of carbonic acid dissolves in water and is only slowly released into the gas phase. The major exogenous factors that determine the rate of gas release are the volume of the solution, the quantity of reactants, the air volume over the reaction mixture, the partial pressure of CO2 of the acid solution before the addition of bicarbonate, and the stirring rate. The presence of food, alcohol, and carbonic anhydrase had relatively little if any effect. Based on our results, we believe that ingestion of the recommended dose of sodium bicarbonate (one-half teaspoon) would result in only small amounts of sudden gas release, probably not enough to be an important factor in causing spontaneous gastric rupture. On the other hand, we measured the amount of sodium bicarbonate that people actually select to take for indigestion, and all exceeded the recommended dose. Some people selected doses of bicarbonate that would result in several hundred milliliters of gas release within 3 min; it seems likely that such injudicious ingestion of sodium bicarbonate, if taken when the stomach was distended with air, food, and liquid, could be an important factor in spontaneous gastric rupture.

Bicarbonates↗

PubMed1993

Safety of low-dose intraoperative bicarbonate therapy: a prospective, double-blind, randomized study. The Study of Perioperative Ischemia (SPI) Research Group.

OBJECTIVES: Recent recommendations suggest that sodium bicarbonate may not be useful for the treatment of metabolic acidosis. However, these recommendations are based primarily on both clinical studies and animal models of metabolic acidosis with arterial hypoxemia (PaO2 of < 80 torr [< 10.7 kPa]). This study was designed to determine the safety and physiologic effects of low-dose sodium bicarbonate in humans who developed intraoperative metabolic acidosis in the absence of hypoxemia. DESIGN: Prospective, double-blind, randomized trial. SETTING: Veterans Affairs Medical Center (a teaching hospital of the University of California, San Francisco). PATIENTS: We prospectively studied 40 patients with coronary artery disease who underwent major surgery and developed mild intraoperative metabolic acidosis (decrease of plasma bicarbonate by > 3 mM). INTERVENTIONS: Patients were randomly assigned to receive either sodium bicarbonate (n = 20) or sodium chloride (n = 20) by intravenous bolus, up to a maximum dose of 88 mmol of sodium. MEASUREMENTS AND MAIN RESULTS: Bicarbonate treatment significantly increased the mean arterial pH from 7.36 to 7.39; the mean serum bicarbonate concentration from 21 to 25 mmol/L; and PCO2 from 41 to 44 torr (5.5 to 5.9 kPa). Total body oxygen consumption and lactate production did not change. Similarly, no adverse changes occurred in systemic or pulmonary arterial pressures or in cardiac ejection fraction. After bicarbonate administration, both the cardiac output and systemic oxygen consumption decreased by 8% to 11%, while both variables increased by 13% after sodium chloride administration; but, none of the changes was significant. One patient in the bicarbonate group developed myocardial ischemia, compared with three patients in the saline group. CONCLUSIONS: Administration of sodium bicarbonate to well-oxygenated patients with mild metabolic acidosis resulted in a correction of the acidosis, without significant changes in cardiac output, total body oxygen use, or PaO2 (oxygen tension). These effects remain to be validated in patients with hypoxemia, more severe acidosis, or less stable circulation.

Acidosis, Lactic↗

PubMed1995

Chloride-bicarbonate exchange through the human red cell ghost membrane monitored by the fluorescent probe 6-methoxy-N-(3-sulfopropyl)quinolinium.

The exchange of chloride and bicarbonate across the human red cell membrane has been characterized by quenching of an intracellular fluorophore, 6-methoxy-N-(3-sulfopropyl)quinolinium (SPQ). In 20 mM Hepes, pH 7.4, and varying concentrations of chloride and bicarbonate with total anion concentration of 150 mM, SPQ is quenched dynamically by chloride with an apparent Stern-Volmer quenching constant 0.071 +/- 0.016 mM-1 at 25 degrees C. Hepes alone quenched SPQ fluorescence with a quenching constant of 0.030 +/- 0.003 mM-1. Stopped-flow kinetic experiments give fluorescence time courses that, when corrected for Stern-Volmer quenching, are first order. Disulfonic stilbenes (inhibitors of anion exchange) decrease the rate of fluorescence equilibration. Transport of bicarbonate via hydration-dehydration of CO2 does not contribute to the observed kinetics. The chloride-bicarbonate exchange rate is independent of the anion concentration gradient, but increases at 25 degrees C from 1 to 4 s-1 as equilibrium chloride concentration increases from 20 to 130 mM (with concomitant decrease in bicarbonate concentration from 130 to 20 mM). The data indicate that the translocation rate of the chloride-loaded transport protein is greater than that of bicarbonate-loaded transport protein and that bicarbonate has a higher affinity for the transport protein than chloride. Our results validate the use of SPQ to measure quantitatively chloride-bicarbonate exchange in red cell ghosts. The methods we describe should be applicable to other systems exhibiting chloride-bicarbonate exchange.

Anions↗

PubMed1984

Evidence for coupled transport of bicarbonate and sodium in cultured bovine corneal endothelial cells.

Using intracellular microelectrode technique, the response of the voltage V across the plasma membrane of cultured bovine corneal endothelial cells to changes in sodium and bicarbonate concentrations was investigated. (1) The electrical response to changes in [HCO3-]o (depolarization upon lowering and hyperpolarization upon raising [HCO3-]o) was dependent on sodium. Lithium could fairly well be substituted for sodium, whereas potassium or choline were much less effective. (2) Removal of external sodium caused a depolarization, while a readdition led to a hyperpolarization, which increased with time of preincubation in the sodium-depleted medium. (3) The response to changes in [Na+]o was dependent on bicarbonate. In a nominally bicarbonate-free medium, its amplitude was decreased or even reversed in sign. (4) Application of SITS or DIDS (10(-3) M) had a similar effect on the response to sodium as bicarbonate-depleted medium. (5) At [Na+]o = 151 mM and [HCO3-]o = 46 mM, the transients of V depended, with 39.0 +/- 9.0 (SD) mV/decade, on bicarbonate and, with 15.3 +/- 5.8 (SD) mV/decade, on sodium. (6) After the preincubation of cells with lithium, replacement of Li by choline led to similar effects as the replacement of sodium by choline, though the response of V was smaller with Li. This response could be reduced or reversed by the removal of bicarbonate or by the application of SITS. (7) Amiloride (10(-3) M) caused a reversible hyperpolarization of the steady-state potential by 8.5 +/- 2.6 mV (SD). It did not affect the immediate response to changes in [Na+]o or [HCO3-]o, but reduced the speed of regaining the steady-state potential after a change in [HCO3-]o. (8) Ouabain (10(-4) M) caused a fast depolarization of -6.8 +/- 1.1 (SD) mV, which was followed by a continuing slower depolarization. The effect was almost identical at 10(-5) M. (9) It is suggested, that corneal endothelial cells possess a cotransport for sodium and bicarbonate, which transports net negative charge with these ions. It is inhibitable by stilbenes, but not directly affected by amiloride or ouabain. Lithium is a good substitute for sodium with respect to bicarbonate transport and is transported itself. In addition, the effect of amiloride provides indirect evidence for the existence of a Na+/H+-antiport. A model for the transepithelial transport of bicarbonate across the corneal endothelium is proposed.

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

PubMedDate not supplied

A role for CagA/VacA in Helicobacter pylori inhibition of murine duodenal mucosal bicarbonate secretion.

Duodenal mucosal bicarbonate secretion is diminished in patients with Helicobacter pylori (HP)-associated duodenal ulcer disease. We examined whether HP water extracts inhibit murine duodenal mucosal bicarbonate secretion in vitro, and the mechanisms involved. Murine duodenal mucosae were mounted in Ussing chambers. Short-circuit current and bicarbonate secretion was measured. CagA/VacA-positive HP water extract (HPWE+/+) markedly inhibited PGE2-, carbachol-, or the calcium ionophore A23187-stimulated bicarbonate secretion in a dose-dependent manner. While 3-isobutyl-1-methylxanthine-stimulated bicarbonate secretion was not affected by HPWE+/+, HPWE+/+ did diminish forskolin-stimulated bicarbonate secretion. HPWE+/+ markedly diminished PGE2-induced increases in duodenal mucosal cAMP. CagA/VacA of HP decreases Ca2+-mediated bicarbonate secretion downstream of increases in intracellular Ca2+. Dimunition of PGE2-stimulated bicarbonate secretion occurs, in part, by inhibition of adenylate cyclase, which leads to decreased cAMP levels. The ability of virulent HP strains to inhibit duodenal bicarbonate secretion through multiple intracellular pathways likely contributes to the pathogenesis of HP-associated duodenal ulcer disease.

Adenylyl Cyclases↗

PubMed1981

Mechanism of bicarbonate action on photosynthetic electron transport in broken chloroplasts.

In CO2-depleted chloroplasts electron transport between the Photosystem II electron acceptor Q and plastoquinone is largely suppressed. In the presence of a high concentration of sodium formate (greater than 10 mM), which probably binds to the bicarbonate site, addition of bicarbonate restores the ferricyanide Hill reaction only after incubation in the dark. With lower formate concentrations bicarbonate is able to restore electron transport in the light. The Hill reaction rate in CO2-depleted chloroplasts after bicarbonate addition, divided by the rate in CO2-depleted chloroplasts before bicarbonate addition, shows a sharp optimum at pH 6.5. Furthermore, the rate-limiting step in bicarbonate action is probably diffusion. The results are explained in terms of a hypothetical model: the bicarbonate-binding site is located at the outer side of the thylakoid membrane, but not directly accessible from the "bulk". To reach the site from the bulk, the molecule has to pass a channel with negatively charge groups on its side walls. In the light these groups are more negatively charged than in the dark. Therefore, the formate ion cannot exchange for bicarbonate in the light, and a dark period is necessary to enable exchange of formate for bicarbonate.

Bicarbonates↗