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At least 811 records · Page 45Linked to original sources
PubMed1985

Kidney epithelial cells of monkey origin (BSC-1) express a sodium bicarbonate cotransport. Characterization by 22Na+ flux measurements.

Na movement across the plasma membranes of confluent monolayers of monkey kidney epithelial cells (BSC-1) was studied using 22Na+ uptake and efflux techniques in the presence of 10(-4) M ouabain. In the presence of 28 mM bicarbonate, uptake was inhibited by both 10(-3) M amiloride and 10(-3) M 4,4'diisothiocyanostilbene-2,2'-disulfonic acid (DIDS). In DIDS-pretreated cells, 10(-3) M amiloride led to a further reduction of 22Na+ uptake, while 10(-5) furosemide was ineffective. DIDS also inhibited sodium efflux, indicating that the DIDS-sensitive pathway mediates both influx and efflux of 22Na+. DIDS-sensitive 22Na+ uptake, as studied in the presence of both 10(-4) M ouabain and 10(-3) M amiloride, was abolished by the absence of bicarbonate, which could not be substituted by other plasma membrane-permeable buffers. In 28 mM HCO3-, DIDS-sensitive uptake of 28 mM Na+ was cis-inhibited by 124 mM Na+, but no significant inhibition by K+ or Li+ was found. DIDS-sensitive 22Na+ uptake was a saturable function of both Na+ concentration (apparent Km between 20 and 40 mM at 28 mM HCO3-) and HCO3- concentration (apparent Km between 7 and 14 mM at 151 mM Na+). Intracellular microelectrode measurements showed that net Na+ transport in the presence of HCO3- is electrogenic, i.e. that there is anion cotransport with Na+. This effect is abolished by 1 mM DIDS. It is concluded that monkey kidney epithelial cells possess a stilbene-sensitive, electrogenic sodium bicarbonate symport, which may play an important role in bicarbonate reabsorption in the mammalian kidney.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1986

Failure of sodium bicarbonate to improve resuscitation from ventricular fibrillation in dogs.

To determine the value of sodium bicarbonate in resuscitation from ventricular fibrillation and the prevention of spontaneous refibrillation, sodium bicarbonate (1 meq/kg) or placebo was administered on a random basis to 16 pentobarbital-anesthetized dogs 18 min after the induction of ventricular fibrillation and cardiopulmonary resuscitation. Defibrillation was attempted 2 min after the administration of bicarbonate or placebo. All animals were successfully defibrillated, but three of eight bicarbonate-treated and two of eight control animals died in electromechanical dissociation (p = NS). Spontaneous refibrillation occurred in three animals in each group (p = NS). Successful resuscitation was not dependent on treatment, arterial or mixed venous Pco2, or arterial or mixed venous pH but correlated strongly with coronary perfusion pressure (p less than .003). Spontaneous refibrillation occurred without relation to any identifiable variable. The gradient between diastolic aortic and right atrial pressures was 24 +/- 2 mm Hg in controls and 23 +/- 2 mm Hg in treated animals over the entire 20 min of cardiopulmonary resuscitation (p = NS). However, among animals successfully resuscitated, mean diastolic coronary perfusion pressure averaged 27 +/- 2 mm Hg compared with 20 +/- 1 mm Hg among those dying in electromechanical dissociation (p less than .02). For the final 2 min of resuscitation, after drug administration, these gradients were 31 +/- 2 and 23 +/- 2 mm Hg, respectively (p less than .01). Microsphere determined myocardial perfusion correlated with the diastolic aortic-right atrial perfusion pressure gradient (r = .86) and was 0.43 +/- 0.03 ml/min/g in survivors and 0.22 +/- 0.01 ml/min/g in nonsurvivors (p less than .01).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Correction of metabolic acidosis in diarrheal calves by oral administration of electrolyte solutions with or without bicarbonate.

Acid-base balance was evaluated in calves with experimentally induced viral diarrhea. When blood pH decreased to less than 7.200, calves were assigned to treatment groups and fed milk replacer, electrolyte solution without bicarbonate, or electrolyte solution containing bicarbonate. Calves in the electrolyte treatment groups had lower mortality (P less than 0.05), were better hydrated (P less than 0.05), and were less acidotic (P less than 0.05) than calves fed milk replacer. Bicarbonate-containing electrolyte solution restored acid-base balance (P less than 0.05) and corrected depression better (P less than 0.05) than electrolyte solution that did not contain bicarbonate. Both electrolyte solutions were equally good at correcting dehydration.

Acidosis↗
PubMed1984

[Animal experiment study on the modification of increased intracranial pressure by THAM (tris-hydroxymethylaminomethane) and sodium bicarbonate].

Intracranial pressure was increased by means of an epidural balloon in 21 young pigs anaesthetised with air/O2 and burprenorphine. Sodium bicarbonate (1 mmol/kg BW) was administered intravenously in 10 animals; THAM (tris-hydroxymethylaminomethane) (1 mmol/kg BW), in 11. Intracranial pressure declined significantly under THAM, from 4.35 kPa in the middle of the infusion to 3.92 kPa at the end, and continued to drop for 15 minutes after its termination. No changes in intracranial pressure, however, were observed in the bicarbonate group. Since mean arterial blood pressure was unchanged in both groups, the increase in cerebral perfusion pressure was significant in the THAM group, but not in the bicarbonate group. Our results, therefore, indicate that THAM is preferable to bicarbonate for correcting acidosis in acute craniocerebral trauma. Controlled ventilation, however, remains indispensable.

Animals↗
PubMed1980

Sodium bicarbonate douching for improvement of the postcoital test.

In the hope of improving sperm survival within the cervical mucus, 93 infertile patients with unfavorable postcoital tests were advised to douche with a solution of sodium bicarbonate 30 to 60 minutes prior to sexual intercourse. In most patients observed, the repeatedly poor postcoital test improved remarkably, and 31 pregnancies have been achieved. In the majority of patients, the postcoital test was repeated on 2 subsequent days (without and with the benefit of sodium bicarbonate douching) with astonishing differences in the test results. In addition to pH changes, sodium bicarbonate douching resulted in significant alteration of the cervical mucus electrolyte components (detected by scanning electron microscopy and energy-dispersive x-ray analysis). The possible modes of action of sodium bicarbonate douching are fully analyzed.

Bicarbonates↗
PubMed1997

Effect of sodium bicarbonate administration on renal function of horses.

OBJECTIVE: To describe changes in renal function of horses after oral and i.v. administration of sodium bicarbonate (NaHCO3) and to determine whether changes are dose dependent. ANIMALS: 6 Standardbred mares. PROCEDURE: Blood and urine samples for determination of renal function were collected immediately before and at hourly intervals for 12 hours after administration of each of 3 oral doses (1,500, 1,000 and 250 mg/kg of body weight, in 3 L of water) and 1 i.v. dose (250 mg/kg, 5% solution) of NaHCO3, or water (3 L orally). RESULTS: NaHCO3 induced increases in urine flow; electrolyte-free water reabsorption; urine concentrations of sodium and bicarbonate; fractional excretion of sodium, potassium, chloride, and bicarbonate; urinary excretion and clearance of sodium and bicarbonate; urine pH and anion gap; and mean plasma concentration of antidiuretic hormone. NaHCO3 induced attenuation in reduction with time of urine excretion and clearance of potassium, chloride, and osmoles, and induced reduction in urine osmolality. Plasma aldosterone and atrial natriuretic peptide concentrations and glomerular filtration rate were not modified. CONCLUSIONS: Renal responses to NaHCO3 load emphasize conservation of plasma volume and reestablishment of acid-base balance over control of hyperosmolality by diuresis, natriuresis, and increased bicarbonaturia. These responses imply a large fluid shift from the extravascular space to the vascular compartment, which was eliminated via diuresis, thus preventing hypervolemia.

Acid-Base Equilibrium↗
PubMedDate not supplied

Hormonal regulation of bicarbonate secretion in the biliary epithelium.

Bicarbonate excretion in bile is a major function of the biliary epithelium. It is driven by the apically located Cl-/HCO3- exchanger which is functionally coupled with a cAMP-dependent Cl- channel (CFTR). A number of hormones and/or neuropeptides with different mechanisms and at different intracellular levels regulate, in concert, the processes underlying bicarbonate excretion in the biliary epithelium. Secretin induces a bicarbonate rich choleresis by stimulating the activity of the Cl-/HCO3- exchanger by cAMP and protein kinase A mediated phosphorylation of CFTR regulatory domain. Protein phosphatase 1/2A are involved in the run-down of secretory stimulus after secretin removal. Acetylcholine potentiates secretin-choleresis by inducing a Ca(++)-calcineurin mediated "sensitization" of adenyl cyclase to secretin. Bombesin and vasoactive intestinal peptide also enhance the Cl-/HCO3- exchanger activity, but the intracellular signal transduction pathway has not yet been defined. Somatostatin and gastrin inhibit basal and/or secretin-stimulated bicarbonate excretion by down-regulating the secretin receptor and decreasing cAMP intracellular levels induced by secretin.

Adenylyl Cyclases↗
PubMed1998

Bicarbonate-mediated social communication stimulates meiosis and sporulation of Saccharomyces cerevisiae.

Meiosis and sporulation in the yeast Saccharomyces cerevisiae requires social communication, mediated by an extracellular factor which is secreted from cells during sporulation and accumulates in a cell density-dependent manner. We show here genetic and biochemical analyses supporting our conclusion that the extracellular factor is bicarbonate acting as an alkali to elevate extracellular pH. Sporulation defects of mdh1 (mitochondrial malate dehydrogenase) mutants and of wild-type cells at low density were rescued extracellularly by addition of bicarbonate or other alkaline solutions to raise medium pH. Addition of bicarbonate (or alkalization of medium) raised steady-state levels of mRNA in respiration-deficient mdh1 mutants and inhibited proliferation of wild-type cells at low density. These results indicate that the two conditions (respiration competency and high cell density), required for meiosis and sporulation, are essential for extracellular accumulation of bicarbonate and resulting alkalization of medium.

Bicarbonates↗
PubMed2005

Pronephric regulation of acid-base balance; coexpression of carbonic anhydrase type 2 and sodium-bicarbonate cotransporter-1 in the late distal segment.

The kidney plays a critical role in regulating the composition of the blood, including pH. The major buffer regulating pH of the blood is bicarbonate. Bicarbonate is freely filtered through the glomerulus and must be recovered from the primary filtrate to maintain appropriate buffering capacity and blood pH. In this report, the expression of carbonic anhydrase type 2 within the late distal segment of pronephroi is described. This expression precisely overlaps that of the sodium-bicarbonate transporter XNBC1. In mammalian kidneys, these two proteins collaborate in the transepithelial recovery of bicarbonate from the kidney filtrate. Coexpression of the genes encoding these proteins in Xenopus embryos indicates that pronephroi use the same recovery system and that this system is largely localized to the late portion of the pronephric distal segment. Not only do the simple pronephroi regulate water and solute balance, they also appear to regulate blood pH in a manner akin to that of the vastly more complex mammalian metanephric kidneys.

Acid-Base Equilibrium↗
PubMed1980

Effect of sodium bicarbonate on in vitro conversion of fibrinogen to fibrin.

The effect of sodium bicarbonate on the conversion of fibrinogen to fibrin clot was investigated using fresh human whole blood and pure human fibrinogen. In vitro experimental data demonstrated that sodium bicarbonate interfered with fibrin clot formation during clotting. This study assessed the possibility of synergistic action of sodium bicarbonate with dosium citrate. As expected, sodium citrate potentiated the anticoagulant action of sodium bicarbonate.

Anticoagulants↗
PubMed1977

Influence of vitamin D on bicarbonate reabsorption.

The effects of acute administration of 25 hydroxycholecalciferol on bicarbonate reabsorption was studied in dogs. 25 hydroxycholecalciferol infused into the renal artery at a dose of 0.2 microgram/kg/hour led to a small but significant bilateral increase in bicarbonate reabsorption in intact dogs. 25 hydroxycholecalciferol had no effect on bicarbonate reabsorption in thyroparathyroidectomized dogs. The phosphaturia of bicarbonate administration was not altered by 25 hydroxycholecalciferol administration.

Animals↗
PubMed1977

Studies on the lithium transport across the red cell membrane. II. Characterization of ouabain-sensitive and ouabain-insensitive Li+ transport. Effects of bicarbonate and dipyridamole.

In studies on Li+ net-transport across the human red cell membrane following results were obtained: 1. In K+- and Na+-free choline chloride media, Li+ is transported into the erythrocytes against an electrochemical gradient. This Li+ uphill transport as well as Li+ downhill transport into the cells is inhibited by ouabain, ATP-depletion, and by external K+ and Na+. The effects of K+ and Na+ are relieved at high Li+ concentrations. 2. Ouabain-sensitive Li+ uptake, determined at 10 mM external Na+, does not obey simple Michaelis-Menten kinetics and exhibits a maximum at about pH 7. 3. Ouabain-resistant Li+ downhill transport into erythrocytes increases with rising pH. It is comprised of a saturating component and a component linearly dependent on external Li+. The linear component is partly inhibited by dipyridamole and accelerated by bicarbonate. The bicarbonate effect can be completely blocked by dipyridamole, phlorizin and phenylbutazone. 4. Li+ release is not inhibited by ouabain, ATP-depletion and external K+. It increases with external Na+ concentration, tending to saturate at 150 mM Na+. Na+-independent Li+ release is stimulated by bicarbonate. It is concluded that ouabain-sensitive Li+ uptake is mediated at the K+-site(s) of the Na+-K+ pump. Li+, K+ and Na+ appear to compete for a common site (or sites). The stimulation of Li+ transfer by bicarbonate and the inhibition by dipyridamole suggest a participation of anionic species in ouabain-resistant Li+ transfer. The Na+-dependent Li+ release and the "saturating component" of Li+ uptake are ascribed to the Na+-dependent Li+ countertransport system.

Adenosine Triphosphate↗
PubMed1984

Electrophysiological analysis of bicarbonate permeation across the peritubular cell membrane of rat kidney proximal tubule. II. Exclusion of HCO3(-)-effects on other ion permeabilities and of coupled electroneutral HCO3(-)-transport.

Cell membrane potentials of rat kidney proximal tubules were measured in response to peritubular ion substitutions in vivo with conventional and Cl- sensitive microelectrodes in order to test possible alternative explanations of the bicarbonate dependent cell potential transients reported in the preceding paper. Significant direct effects of bicarbonate on peritubular K+, Na+, and Cl- conductances could be largely excluded by blocking K+ permeability with Ba2+ and replacing all Na+ and Cl- by choline or respectively SO4(2-) isethionate, or gluconate. Under those conditions the cell membrane response to HCO3- was essentially preserved. In addition it was observed that peritubular Cl- conductance is negligibly small, that Cl-/HCO3- exchange - if present at all - is insignificant, and that rheogenic HCO3- flow with coupling to Na+ flow is also absent or insignificant. A transient disturbance of the Na+ pump or a transient unspecific increase of the membrane permeability was also excluded by experiments with ouabain and by the observation that SITS (4-acetamido-4'-isothiocyano-2,2' disulphonic stilbene) blocked the HCO3- response instantaneously. The data strongly support the notion that the potential changes in response to peritubular HCO3- concentration changes arise from passive rheogenic bicarbonate transfer across the peritubular cell membrane, and hence that this membrane has a high conductance for bicarbonate buffer.

4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfo↗
PubMed1980

Adrenergic control of bicarbonate absorption in the proximal convoluted tubule of the rat kidney.

The effects of norepinephrine and phenoxybenzamine on bicarbonate absorption in the rat proximal convoluted tubules were studied by simultaneous microperfusion of tubule and peritubular capillaries. Bicarbonate was determined by using a pH-sensitive membrane electrode system. The rates of bicarbonate absorption (JHCO3) were examined in the same proximal tubule before and after the addition of norepinephrine or phenoxybenzamine. When the proximal tubule was perfused with Ringer solution and peritubular capillaries were perfused with albumin Ringer solution, JHCO3 was 145 +/- 3.3 pEq/min X mm. Addition of 2 X 10(-6) mol/l norepinephrine to the capillary perfusate caused a 21% increase in JHCO3. Addition of 2 X 10(-6) mol/l phenoxybenzamine to the capillary perfusate caused a 12% decrease in JHCO3. Addition of both norepinephrine and phenoxybenzamine to the capillary perfusate caused a 19% decrease in JHCO3. However, there was no significant effect on JHCO3 observed when either norepinephrine or phenoxybenzamine was added to the luminal perfusate. These results suggest that adrenergic nerves participate in the regulation of renal tubular bicarbonate absorption through the direct action of norepinephrine on adrenergic receptors located at the basolateral side of the proximal tubule.

Absorption↗
PubMed1990

Time- and dose-dependent effects of protein kinase C on proximal bicarbonate transport.

Activation of protein kinase C has been shown to cause both stimulation and inhibition of transport processes in the brush-border membrane and renal tubule. This study was designed to examine the dose-response nature and time-dependent effect of 4 beta-phorbol-12-myristate-13-acetate (PMA) on the rates of bicarbonate absorption (JHCO3) and fluid absorption (Jv) in the proximal convoluted tubule (PCT) of rat kidney. Bicarbonate flux was determined by total CO2 changes between the collected fluid and the original perfusate as analyzed by microcalorimetry. Luminal perfusion of PMA (10(-10) approximately 10(-5) M) within 10 min caused a significant increase of JHCO3 and Jv. A peaked curve of the dose response was observed with maximal effect at 10(-8) M PMA on both bicarbonate and fluid reabsorption, which could be blocked completely by amiloride (10(3) M) and EIPA (10(-5) M). On the other hand, with an increase of perfusion time beyond 15 min. PMA (10(-8) and 10(-6) M) could inhibit JHCO3 and Jv. Amiloride (10(-3) M) or EIPA (10(-5) M) significantly inhibits JHCO3 and Jv, while there is no additive effect of PMA and amiloride or EIPA on PCT transport. An inactive phorbol-ester, 4 alpha-phorbol, that does not activate protein kinase C, had no effects on JHCO3 and Jv. Capillary perfusion of PMA (10(-8) M) significantly stimulate both JHCO3 and Jv; however, PMA did not affect glucose transport from either the luminal side or basolateral side of the PCT. These results indicate that activation of endogenous protein kinase C by PMA could either stimulate or inhibit both bicarbonate and fluid reabsorption in the PCT dependent on time and dose, and these effects are through the modulation of Na+/H+ exchange mechanism.

Amiloride↗
PubMed1984

Electrical effects of potassium and bicarbonate on proximal tubule cells of Necturus.

The effects of stepwise concentration changes of K+ and HCO3- in the basolateral solution on the basolateral membrane potential (Vbl) of proximal tubule cells of the doubly-perfused Necturus kidney were examined using conventional microelectrodes. Apparent transference numbers were calculated from changes in Vb1 after alterations in external K+ concentration from 1.0 to 2.5 mM (tK, 1.0-2.5), 2.5 to 10, and in external HCO3- concentration (at constant pH) from 5 to 10 mM (tHCO3, 5-10), 10 to 20, or 10 to 50. tK, 2.5-10 was 0.38 +/- 0.02 under control conditions but was sharply reduced to 0.08 +/- 0.03 (P greater than 0.001) by 4 mM Ba++. This concentration of Ba++ reduced Vb1 by 9 +/- 1 mV (at 2.5 external K+). Perfusion with SITS (5 X 10(-4)M) for 1 hr hyperpolarized Vb1 by 10 +/- 3 mV and increased tK, 2.5-10 significantly to 0.52 +/- 0.01 (P less than 0.001). Ba++ application in the presence of SITS depolarized Vb1 by 22 +/- 3 mV. In control conditions tHCO3, 10-50 was 0.63 +/- 0.05 and was increased to 0.89 +/- 0.07 (P less than 0.01) by Ba++ but was decreased to 0.14 +/- 0.02 (P less than 0.001) by SITS. In the absence of apical and basolateral chloride, the response of Vb1 to bicarbonate was diminished but still present (tHO3, 10-20 was 0.35 +/- 0.03). Intracellular pH, measured with liquid ion-exchange microelectrodes, increased from 7.42 +/- 0.19 to 7.57 +/- 0.17 (P less than 0.02) when basolateral bicarbonate was increased from 10 to 20 mM at constant pH. These data show that the effects of bicarbonate on Vb1 are largely independent of effects on the K+ conductance and that there is a significant current-carrying bicarbonate pathway in the basolateral membrane.(ABSTRACT TRUNCATED AT 250 WORDS)

4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfo↗
PubMed1996

Bicarbonate dependence of ion current in damaged bone.

The aim of this work was to characterize the ion current that enters mouse metatarsal bones following damage to the cortex. We assessed both the spatial distribution of this current and its dependence on the presence of bicarbonate in the medium. We used a voltage-sensitive probe system vibrating in two dimensions and recorded the signal as function of the position of the probe with respect to the site of damage and of ion substitutions in the medium. When the cortex was damaged (50 microm cylindrical hole penetrating into the marrow cavity), we recorded a steady state net inward electrical current directed toward the site of damage. In nonbicarbonate media, the density of the current was maximal near the center of the hole and ranged from 6 to 18 microA/cm2. As the probe was moved off the center of the hole, measured current density decreased in a manner consistent with the hypothesis that the source of the inward current is localized to the hole. After changing bicarbonate concentration in the medium from 0 to 42 mM, the current density nearly doubled, then decayed back to its original level exponentially over 35 minutes. When the diaphysis of living bone was left intact the current density was close to background level either in the presence or absence of bicarbonate in the medium. Damaged dead bone did not drive any current higher than background level. We conclude that the vibrating probe technique is a powerful tool to characterize ion currents in injured bone, helping to understand the physiology of bone-plasma interface and the bone healing processes. The current density transiently doubled upon addition of bicarbonate, indicating that this ion may carry the electrical current in damaged bone, probably by pump-leak mechanisms operating at the bone-plasma interface.

Animals↗
PubMed1989

Effect of 15(R)-15-methyl PGE2 (arbaprostil) on duodenal bicarbonate secretion in rat.

The present study was designed to observe the effect of 15(R)-15-methyl PGE2 (arbaprostil) on duodenal bicarbonate secretion in male Wistar rats anesthetized with urethane. A proximal duodenal loop (1.5cm) was made and perfused with saline (pH4.5) in an air tight circle system. The pH and Pco2 of the perfusing fluid were measured continuously and the quantity of bicarbonate was calculated according to the Henderson-Hasselbalch equation. Vehicle or arbaprostil was injected intravenously as a bolus injection. The total output of bicarbonate in 30 min was as follows; control: 0.449 +/- 0.093 microEq (mean +/- SE); 1,10 and 100 mu/kg of arbaprostil: 0.752 +/- 0.218, 2.75 +/- 0.430 and 5.958 +/- 0.578 microEq respectively. Arbaprostil (10 and 100 micrograms/kg) increased the total output of bicarbonate significantly (p less than 0.001). The rate of secretion was also increased by arbaprostil.

Animals↗