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PubMed1989

Effects of sodium bicarbonate or sodium sesquicarbonate on lactating Holsteins fed a high grain diet.

Fifteen Holstein cows, 35 to 70 d postpartum, were assigned to five 3 x 3 Latin squares. Treatments were: control (60% concentrate, 40% corn silage, DM basis) or control supplemented with either .71% sodium bicarbonate or .65% sodium sesquicarbonate, DM basis. Orthogonal contrasts compared the effect of both buffered diets versus the control diet, and the effect of sodium bicarbonate supplementation vs. sodium sesquicarbonate supplementation. There were no differences among treatments for milk yield (34.9 kg/d), milk fat yield (.99 kg/d), 3.5% FCM (31.1 kg/d), or milk protein concentration (3.15%). There were no treatment effects on total chewing time. Milk fat concentration tended to be greater for cows fed sodium bicarbonate (2.92%) and sodium sesquicarbonate (2.89%) relative to control (2.82%). Relative to control, sodium bicarbonate and sodium sesquicarbonate supplementation increased DM intake (22.0 and 22.7 vs. 21.4 kg/d), digestible DM intake (16.7 and 16.2 vs. 14.8 kg/d), digestible organic matter intake (16.0 and 15.5 vs. 14.3 kg/d); and apparent digestibility of DM (77.3 and 74.8 vs. 73.3%) and NDF (62.6 and 56.5 vs. 54.7%). Relative to sesquicarbonate, bicarbonate supplementation increased apparent digestibilities of CP (82.3 vs. 78.8%) and NDF, and decreased milk protein yield (1.06 vs. 1.11 kg/d). Sesquicarbonate was as effective as bicarbonate in alleviating milk fat depression and increasing intake of digestible organic matter.

Animals↗
PubMed1992

Sodium bicarbonate and yeast culture effects on ruminal fermentation, growth, and intake in dairy calves.

Sodium bicarbonate and yeast culture effects on ruminal fermentation, intake, and growth were evaluated in young calves. In trail 1, nine ruminally cannulated Holstein calves averaging 12 wk of age were fed control starter (17% CP) or starters containing 3% sodium bicarbonate or .2% yeast (Saccharomyces cerevisiae) culture in a 3 x 3 Latin square. Calves were fed for ad libitum consumption for 10 d and then at 85% of ad libitum intake to d 14. Ruminal fluid taken at 0 h postfeeding tended to have higher pH and a greater proportion of acetate when calves were fed sodium bicarbonate, but other ruminal and blood parameters did not differ among treatments. By 4 h after feeding, ruminal VFA had increased to 120.7 mM, molar proportions of individual acids were altered, and blood ketones and VFA increased in treated calves. In trial 2, 42 Jersey calves were fed experimental starters for ad libitum consumption during a 12-wk study. Calves began the study at 3 to 5 d of age. There were no significant effects of yeast culture or sodium bicarbonate on DMI or intake of starter, rates of gain, or feed efficiency. Plasma urea N was reduced when sodium bicarbonate was fed. Both sodium bicarbonate and yeast culture affected blood and ruminal metabolites when calves were limit-fed but did not influence intake or daily gain when calves were fed for ad libitum consumption.

Animal Feed↗
PubMed1986

Utilization of sodium from sodium bicarbonate by broiler chicks.

Two experiments were performed with broiler chicks housed in battery brooders to ascertain their response to low levels of dietary sodium, supplied by either sodium chloride or sodium bicarbonate, and to compare the utilization of sodium from the materials. In each experiment, three replicate pens containing seven female day-old chicks were offered each treatment for a 21-day feeding period. Sodium chloride levels of 0, .05, .10, .15, or .20% were a portion of the dietary treatments. Additional groups received the same basal supplemented with .072, .144, or .216% sodium bicarbonate in the first experiment and .072 or .144% during the second, in order to provide sodium levels comparable to those resulting from .05, .10, or .15% sodium chloride. Group body weights, water consumption, feed consumption, and manure moisture served as evaluation criteria. As the level of sodium chloride was increased, body weights, feed and water intake, and manure moisture also increased. In neither experiment were there significant differences between the body weights of birds receiving sodium bicarbonate and those resulting from feeding comparable levels of sodium from sodium chloride. Average daily feed and sodium intake also did not differ statistically between groups receiving comparable sodium from either source. Water intake tended to be somewhat higher for sodium bicarbonate treatments and was significantly so for the .144% sodium bicarbonate treatment of the second experiment. Manure moisture was somewhat variable and did not differ statistically between sources at the same sodium level. It is concluded that the sodium from sodium bicarbonate was utilized in a manner comparable to that from sodium chloride.

Animals↗
PubMed1999

Effect of glandular kallikrein on distal bicarbonate transport. Role of basolateral Cl-/HCO3- exchanger and vacuolar H(+)-ATPase.

The luminal membrane of collecting duct cells, specially the intercalated cells, is normally exposed to active kallikrein. This is due to the specific localization of renal kallikrein in the connecting tubule cells. We have previously reported inhibition of distal bicarbonate secretion by renal kallikrein. The present study was performed to evaluate the participation of basolateral Cl-/HCO3- exchanger and luminal H(+)-ATPase activity of cortical collecting duct segments (CCD) in the mechanism involved in the inhibition of bicarbonate secretion induced by the enzyme. The effect of orthograde injections of 1 microgram/ml (250 U/6.3 mg) pig pancreatic kallikrein, in the absence and presence of 1 mM DIDS (stilbene-disulfonic acid) in the renal tubule system, was evaluated. Urine fractions were collected after two-minutes stop-flow. Changes in the urine fraction (Fr) related to those in free-flow urine samples (Ff) were related to the respective polyfructosan (Inutest) ratio. Renal kallikrein activity (Fr:Ff kallikrein/Fr:Ff polyfructosan) increased significantly in the first 120 microliters urine fraction collected after glandular 1 microgram/ml kallikrein, P < 0.05, (first stop-flow) and after glandular 1 microgram/ml kallikrein plus 1 mM. DIDS P < 0.05 (second stop flow). Bicarbonate secretion rate (Fr:Ff HCO3-/Fr:Ff polyfructosan) of collecting ducts was significantly reduced in the first 120 microliters urine fraction collected, related to control, during the first and second stop-flow periods. No difference was shown in bicarbonate excretion between the first 120 microliters urine fractions collected after administration of glandular kallikrein and glandular kallikrein plus DIDS. To measure H(+)-ATPase activity, rat microdissected cortical collector tubules (CCD) were incubated in the presence of increasing glandular kallikrein doses (A: 93, B: 187 and C: 375 mU/200 microL) in the presence of ouabain (4 microM) and omeprazole (100 microM) to inhibit Na(+)-K(+)-ATPase and H(+)-K(+)-ATPase, respectively. In CCD, bafilomycin-sensitive H(+)-ATPase activity (pmol/mm/min) after increasing kallikrein doses did not differ significantly from control. No difference related to control H(+)-ATPase activity was observed when microdissected CCD segments were incubated in the presence of an AT1 receptor antagonist (Losartan 10(-6) M) and glandular kallikrein (93 mU). On the contrary, angiotensin II (10(-8) M) significantly decreased H(+)-ATPase activity. The present study shows that neither basolateral Cl-/HCO3- exchanger nor H(+)-ATPase activity are involved in bicarbonate inhibition by glandular kallikrein at CCD. Involvement of luminal Cl-/HCO3- exchanger at beta intercalated cells in CCD may be suggested for the bicarbonate secretion inhibition induced by renal kallikrein.

Animals↗
PubMed1985

Sodium bicarbonate in seminal plasma stimulates the motility of mammalian spermatozoa through direct activation of adenylate cyclase.

Recently, a low molecular weight factor, which specifically stimulates sperm adenylate cyclase, was found in porcine seminal plasma (Okamura, N., and Sugita, Y. (1983) J. Biol. Chem. 258, 13056-13062). The purified factor was analyzed by 1H NMR, 13C NMR, infrared spectroscopy, and elementary analysis and identified as sodium bicarbonate. The effects of sodium bicarbonate both on adenylate cyclase activity in porcine spermatozoa and on sperm motility have been studied. Sperm adenylate cyclase was found to be specifically activated by bicarbonate over the physiological concentration range. In contrast, the adenylate cyclase activity in other tissues was not affected. The same concentration range of bicarbonate which resulted in activation of adenylate cyclase also stimulated sperm motility. The motility and enzyme activity of spermatozoa in all species so far tested (human, bovine, rat, mouse, and dog) were found to be similarly sensitive to bicarbonate concentration. These results show that the bicarbonate-sensitive adenylate cyclase system regulates sperm motility and suggest that this system is common to all mammals.

Adenylyl Cyclases↗
PubMed1984

The effect of the bicarbonate anion on serum ionized calcium concentration in vitro.

The effect of changes in bicarbonate ion concentration on calcium ion concentration was examined in vitro in serum and protein-free solution. The findings in this study support the formation of a calcium-bicarbonate complex (CaHCO3+) that has a KA of 5.20 in protein-free solution. [Ca++] varied inversely with [HCO3-] in both serum and protein-free solution. This variation was independent of the known variation of [Ca++] with pH. In serum [Ca++] varied 0.0036 mM Ca++ per 1 mM change in [HCO3-] compared with a variation of 0.0060 mM Ca++ per 0.01 unit change in pH. Addition of bicarbonate to serum (Pco2 constant) produced a 50% greater decrease in [Ca++] than that produced by a reduction in Pco2 which gave the same pH change. These findings indicate that abnormal bicarbonate concentrations should be considered when ionized calcium concentrations are estimated from total plasma calcium values in acid-base disorders. In metabolic acid-base disorders, the bicarbonate effect adds to the pH effect on calcium ion concentration. In compensated respiratory acid-base disorders, the bicarbonate effect subtracts from the pH effect on calcium ion concentration.

Acid-Base Imbalance↗
PubMed1993

The effects of different doses of sodium bicarbonate on the absorption and activity of non-micronized glibenclamide.

The effects of different doses of sodium bicarbonate on the absorption and activity of non-micronized glibenclamide were studied in six healthy volunteers, using a randomized crossover design with four phases. The subjects ingested a single dose of non-micronized glibenclamide (2.5 mg) with 150 ml of water or with 150 ml of water containing 0.3, 1.0 or 3.0 g of sodium bicarbonate. Plasma concentrations of glibenclamide, insulin and glucose were measured. Coadministration of 1.0 or 3.0 g of sodium bicarbonate with non-micronized glibenclamide increased the area under the plasma glibenclamide concentration-time curve (AUC) from 0 to 1 h 30-fold (p < 0.05) and 38-fold (p < 0.05), respectively. The 1.0- and 3.0-g doses of sodium bicarbonate also increased the AUC of plasma glibenclamide from 0 to 2 h, about 3-fold (p = 0.05 and 0.07, respectively). The peak plasma concentration, peak time and total extent of absorption of glibenclamide and the insulin and glucose responses were not significantly altered by any of the doses of sodium bicarbonate studied. Concomitant ingestion of 1.0 or 3.0 g of sodium bicarbonate and non-micronized glibenclamide greatly increased the early bioavailability of glibenclamide. However, this interaction did not alter the activity of glibenclamide.

Adult↗
PubMed2006

Sodium bicarbonate infusion during resuscitation of infants at birth.

BACKGROUND: For many years, intravenous sodium bicarbonate has been used to reverse acidosis during newborn resuscitation. However, controversy surrounds its use. Most of the evidence has been derived from studies in animals, adult humans, or in uncontrolled, descriptive experiments. Despite the lack of evidence from the human neonatal population and concerns about its safety, some international resuscitation guidelines still recommend the use of sodium bicarbonate in resuscitation of the newborn. OBJECTIVES: To determine whether an intravenous infusion of sodium bicarbonate, compared to placebo or no treatment, reduces mortality and morbidity (in particular regarding neurodevelopmental outcome) in infants receiving resuscitation in the delivery room at birth. SEARCH STRATEGY: We used the standard search strategy of the Cochrane Neonatal Review Group. Searches were conducted of the Cochrane Central Register of Controlled Trials (CENTRAL, The Cochrane Library, Issue 3, 2005), MEDLINE (1966 - September 2005), EMBASE (1980 - September 2005) and CINAHL (1982 - September 2005) and Pediatric Research (1987 - September 2005). Unpublished trials were sought by handsearching the conference proceedings of American Pediatric Society/Society for Pediatric Research (1990 - 2005) and European Society for Paediatric Research (1993 - 2005). SELECTION CRITERIA: Randomised or quasi-randomised controlled trials of newborn infants receiving sodium bicarbonate infusion during any resuscitation in the delivery room at birth. DATA COLLECTION AND ANALYSIS: Two review authors independently assessed trial quality and extracted data. Study authors were contacted for additional information. MAIN RESULTS: We found one randomised controlled trial that fulfilled the eligibility criteria (Lokesh 2004) that compared treating asphyxiated newborn infants (infants continuing to need positive pressure ventilation at 5 minutes after birth) with sodium bicarbonate infusion (N = 27) versus 5% dextrose (N = 28). They found no evidence of an effect on mortality prior to discharge [Relative risk 1.04 (95% confidence interval 0.49 to 2.21)], abnormal neurological examination at discharge [Relative risk 0.86 (95% confidence interval 0.30 to 2.50)] or a composite outcome of death or abnormal neurological examination at discharge [Relative risk 0.97 (95% confidence interval 0.59 to 1.60)]. There was no statistically significant difference in the incidence of encephalopathy [Relative risk 1.30 (95% confidence interval 0.88 to 1.92)], intraventricular haemorrhage [Relative risk 1.04 (95% confidence interval 0.23 to 4.70)] and neonatal seizures [Relative risk 1.19 (95% confidence interval 0.50 to 2.82)]. No long term neurodevelopmental outcomes were assessed. AUTHORS' CONCLUSIONS: There is insufficient evidence from randomised controlled trials to determine whether the infusion of sodium bicarbonate reduces mortality and morbidity in infants receiving resuscitation in the delivery room at birth.

Asphyxia Neonatorum↗
PubMed1995

Flow cytometric detection of bicarbonate-induced changes in lectin binding in boar and ram sperm populations.

Boar and ram spermatozoa were incubated in Tyrode's medium in the presence or absence of bicarbonate/CO2, a component believed essential for capacitation. At intervals, samples were stained with a range of FITC-lectins to detect changes in surface glycoconjugates, using a rapid staining technique to avoid problems of lectin toxicity. The samples were then analysed directly by flow cytometry, using propidium iodide to distinguish dead cells. In the presence of bicarbonate, a live subpopulation of spermatozoa developed, which in both animal species showed higher binding affinities towards Phaseolus Vulgaris Agglutinin (PHA-E), Sophora Japonica Agglutinin (SJA), and Soybean Agglutinin (SBA), and lower binding affinity towards Erythrina Cristagalli Lectin (ECL). In boar samples, the modified subpopulation reached a maximum after 3 hr incubation, whereas in ram samples it maximized after 1.5 hr. No changes were seen when spermatozoa were incubated in bicarbonate-free medium. The bicarbonate-induced changes in lectin binding were not due to the onset of acrosome reactions, because spermatozoa induced to undergo acrosome reactions with the ionophore A23187 displayed very different lectin-binding patterns. Tested on boar spermatozoa, seminal plasma not only inhibited but reversed the bicarbonate-induced development of the modified subpopulation. EGTA also inhibited development of boar sperm subpopulations; excess Ca2+ was unable to overcome this inhibition, suggesting that multivalent metal ions might be involved in bicarbonate's action. We conclude that bicarbonate causes a loss of surface coating material with affinity for ECL and an unmasking of binding sites for SBA, SJA and PHA-E. A modified subpopulation of live spermatozoa is thereby established, which appears to maximize at a rate in accord with reported capacitation times.

Animals↗
PubMed1994

Complementary Mössbauer and EPR studies of iron(III) in diferric human serum transferrin with oxalate or bicarbonate as synergistic anions.

The spectral and magnetic properties of iron(III) bound in the metal binding sites of human serum transferrin with oxalate or bicarbonate as synergistic anions has been studied with Mössbauer spectroscopy and electron paramagnetic resonance (EPR). The Mössbauer spectra of the iron(III) in diferric transferrin with oxalate have been described using a spin Hamiltonian with the values of the zero field splitting parameter, D = 0.55 +/- 0.05 cm-1, and the rhombicity of the crystal field, E/D = 0.045 +/- 0.005. The EPR spectrum can be described with D = 0.58 cm-1 and E/D = 0.057, using a g-strain model for the lineshape that is based on a Gaussian distribution of D and E/D with Gaussian widths sigma(D) = 0.35 cm-1 and sigma(E/D) = 0.013, respectively. The rhombicity of the iron surroundings for the transferrin-oxalate complex is almost one order of magnitude smaller than for the bicarbonate complex and the zero field splitting parameter is twice as large in the oxalate as in the bicarbonate complex. We conclude that the crystal field symmetry of the iron site is almost tetragonal in the oxalate complex but rhombohedral in the bicarbonate complex, reflecting the different geometries of the oxalate and bicarbonate coordination. The isomer shift delta = 0.56 +/- 0.01 mm s-1 and the quadrupole splitting delta EQ = 0.2 +/- 0.1 mm s-1, on the other hand, are very close to the values found for the bicarbonate complex. No differences between the Mössbauer spectra of the two iron(III) ions in diferric transferrin with oxalate were found. The homogeneity of the diferric transferrin samples was controlled by capillary zone electrophoresis in the presence of urea.

Bicarbonates↗
PubMed1975

pH and bicarbonate excretion in the rat parotid gland as a function of salivary rate.

The bicarbonate concentration in rat parotid saliva increases with increasing flow rates and approximates plasma values at highest salivation. At lowest flow rates the bicarbonate concentration in the secretory fluid markedly exceeds the plasma levels. Intravenous administration of acetazolamide has no influence on the bicarbonate excretion of the parotid gland. Following retrograde application of acetazolamide into the gland duct the concentrations of both bicarbonate and sodium are elevated. The potassium concentrations in final saliva exceed 70 mEq/l at flow rates below 5 mul/min g gland weight. With increasing flow rates a precipitous decrease in potassium concentration below 10 mEq/l occurs. With further increase in flow rate the potassium concentration remains unchanged. The sodium concentrations increased with augmented salivation rate. At lowest flow rates the sodium concentrations showed an increase of modest degree. Our findings can best be explained by the existence of two independent ductular mechanism: a) bicarbonate reabsorption probably in the striated ducts of the parotid gland; b) secretion of potassium with concomitand secretion of bicarbonate in the main excretory duct.

Acetazolamide↗
PubMed1977

The placental transfer of lactate and bicarbonate in the guinea-pig.

In order to study the lactic acid transfer in a hemochorial placenta, the placenta of the guinea-pig was perfused in situ through the umbilical circulation with a colloidal solution containing L(+)-lactate and bicarbonate in various concentrations. It was found that the transfer rates of lactate and bicarbonate were proportional to the respective materno-fetal arterial concentration differences. When the concentration gradients for lactate and bicarbonate were opposite to each other, an exchange of lactate for bicarbonate occurred which is equivalent to a lactic acid transfer. The placental permeability for lactate was found to be 25 micronmol(h - micronmol/ml) per g of placental weight (S.E. = 2). A similar value was obtained for bicarbonate (23 micronmol/(h - micronmol/ml) per g; S.E. = 1.3). It is calculated that fetal concentrations of lactate and bicarbonate follow maternal concentration changes with a half time of 23 min.

Animals↗
PubMed1977

The influence of carbon dioxide, bicarbonate and other buffers on the potential of antimony microelectrodes.

Antimony microelectrodes were calibrated at 37 degrees C in phosphate buffers, in different bicarbonate solutions at various CO2-partial pressures and in buffers like TRIS1, TES2, MES3 and malonic acid. By use of the latter buffers (with exception of malonic acid) the most reliable calibration curves were obtained ("normal values"). The usual calibration in 67 mmol/l standard phosphate buffers turned out to be unacceptable because the obtained mV-values were too high (negative) in comparison to all other buffers. Different calibration curves resulted from the use of pure bicarbonate solution whether the pH-values were changed by variation of pCO2 or of the bicarbonate concentration. Low bicarbonate concentrations in combination with low pCO2 gave mV-values which were too low relative to the other buffers. Both the increase of pCO2 as well as of the bicarbonate concentration caused a shift of the potential of the antimony electrodes toward "normal values". In solutions containing other buffers the influence of bicarbonate and pCO2 became negligible with increasing buffer concentration. Decreasing oxygen partial pressure was found to cause an increase of the potential of the antimony electrodes. The influence of liquid junction potentials at the reference electrode is discussed.

Antimony↗
PubMed2001

Effects of sodium bicarbonate supplementation on axial and peripheral bone mass in rats on strenuous treadmill training exercise.

We observed the effects of sodium bicarbonate supplement on bone mass in rats on strenuous treadmill training. Sixty female Wistar rats (93-days-old; mean initial weight 261 +/- 16 g) were studied. One group of 15 rats was killed at the beginning of the experiments (basal control group), while another group of 15 rats was not manipulated (Exer-NaB-). Another group of 15 rats was exercised but did not receive sodium bicarbonate (Exer+NaB-), while the final group of 15 rats exercised and received sodium bicarbonate (Exer+NaB+) at a dose of 0.05 mg/kg/day, administered by esophageal catheter on exercise days. These rats were killed at the end of 11 weeks. Femoral and vertebral length, weight, and bone mineral content (BMC) and density (BMD) were measured. According to ANOVA with the Tukey-Kramer test, femur length and weight, vertebral weight, femur BMC and BMD, vertebral BMC and BMD and the ratio between femur and vertebral BMC and final body weight, and plasma bicarbonate were lower in the basal control and Exer+NaB- groups than in the two other groups (P < 0.005-0.0001). Overall, there was a positive correlation between femur and vertebral BMC and femur BMC and length (P < 0.0001 for all). Only in the Exer+NaB- group was there a positive association between plasma bicarbonate levels and femur length (r = 0.78; P < 0.0005). Our study demonstrates the adverse effects of strenuous exercise on bone, and the usefulness of sodium bicarbonate supplements in preventing and minimized these effects.

Animals↗
PubMed1984

Gas exchange during dialysis. Contrasting mechanisms contributing to comparable alterations with acetate and bicarbonate buffers.

Although arterial hypoxemia during hemodialysis is common and may contribute to dialysis morbidity, the mechanisms responsible remain uncertain. Additionally, controversy exists as to whether bicarbonate dialysate produces less hypoxemia than acetate dialysate. The short- and long-term effects of acetate dialysate and bicarbonate dialysate on gas exchange were compared in eight stable patients undergoing dialysis using a closed, proportioning system and a double-blind, crossover study design. Dialysate was sampled immediately proximal and distal to the dialyzer to determine its contribution to total carbon dioxide elimination. Ventilatory parameters and blood gas values were measured before dialysis, at one hour, and after dialysis. Arterial oxygen tension fell significantly and comparably at one hour with both dialysates, whereas the alveolar-arterial oxygen gradient increased only slightly. Despite hypoxemia, minute ventilation decreased by 4 to 18 percent, and arterial carbon dioxide tension was unchanged. Although total carbon dioxide elimination was unchanged in all groups, there was a significant decrease in lung total carbon dioxide elimination with acetate dialysate of 9.23 +/- 2.69 to 7.74 +/- 1.57 mmol per minute on Day 1 (mean +/- SD, p less than 0.025) concomitant with a loss of total carbon dioxide into the bath of 2.04 +/- 0.20 mmol per minute, resulting in a significant reduction in respiratory quotient (0.92 +/- 0.07 to 0.75 +/- 0.05, p less than 0.01). In contrast, there was a gain of total carbon dioxide into the blood of 1.64 +/- 0.45 mmol per minute with bicarbonate dialysate, which resulted in an increased pH at one hour compared with acetate dialysate (7.39 +/- 0.04 versus 7.35 +/- 0.03, p less than 0.05). Hypoxemia persisted after dialysis in all groups and was associated with an increased alveolar-arterial oxygen gradient in three of the four groups. It is concluded that transitory hypoventilation contributes to comparable hypoxemia with both acetate and bicarbonate dialysates by different mechanisms. With acetate dialysate, there is a decrease in carbon dioxide load to the lungs, whereas with bicarbonate dialysate, the mechanism responsible appears to be a suppression of respiratory drive resulting from a gain of bicarbonate from the dialysate. Additionally, neither dialysate prevents post-dialysis hypoxemia, which is associated with an increased alveolar-arterial oxygen gradient resulting from a mechanism that remains to be elucidated.

Acetates↗
PubMed1992

Is bicarbonate in Photosystem II the equivalent of the glutamate ligand to the iron atom in bacterial reaction centers?

Photosystem II of oxygen-evolving organisms exhibits a bicarbonate-reversible formate effect on electron transfer between the primary and secondary acceptor quinones, QA and QB. This effect is absent in the otherwise similar electron acceptor complex of purple bacteria, e.g., Rhodobacter sphaeroides. This distinction has led to the suggestion that the iron atom of the acceptor quinone complex in PS II might lack the fifth and sixth ligands provided in the bacterial reaction center (RC) by a glutamate residue at position 234 of the M-subunit in Rb. sphaeroides RCs (M232 in Rps. viridis). By site-directed mutagenesis we have altered GluM234 in RCs from Rb. sphaeroides, replacing it with valine, glutamine and glycine to form mutants M234EV, M234EQ and M234EG, respectively. These mutants grew competently under phototrophic conditions and were tested for the formate-bicarbonate effect. In chromatophores there were no detectable differences between wild type (Wt) and mutant M234EV with respect to cytochrome b-561 reduction following a flash, and no effect of bicarbonate depletion (by incubation with formate). In isolated RCs, several electron transfer activities were essentially unchanged in Wt and M234EV, M234EQ and M234EG mutants, and no formate-bicarbonate effect was observed on: (a) the fast or slow phases of recovery of the oxidized primary donor (P+) in the absence of exogenous donor, i.e., the recombination of P+Q-A or P+Q-B, respectively; (b) the kinetics of electron transfer from Q-A to QB; or (c) the flash dependent oscillations of semiquinone formation in the presence of donor to P+ (QB turnover). The absence of a formate-bicarbonate effect in these mutants suggests that GluM234 is not responsible for the absence of the formate-bicarbonate effect in Wt bacterial RCs, or at least that other factors must be taken into account. The mutant RCs were also examined for the fast primary electron transfer along the active (A-)branch of the pigment chain, leading to reduction of QA. The kinetics were resolved to reveal the reduction of the monomer bacteriochlorophyll (tau = 3.5 ps), followed by reduction of the bacteriopheophytin (tau = 0.9 ps). Both steps were essentially unaltered from the wild type. However, the rate of reduction of QA was slowed by a factor of 2 (tau = 410 +/- 30 and 47 +/- 30 ps for M234EQ and M234EV, respectively, compared to 220 ps in the wild type).(ABSTRACT TRUNCATED AT 400 WORDS)

Benzoquinones↗
PubMed1990

Stimulation of duodenal bicarbonate secretion in conscious rats by cerebral somatostatin-28. Role of neurohumoral pathways.

The central nervous system effects of somatostatin-28 on proximal duodenal bicarbonate secretion were studied in freely moving rats. Cerebroventricular administration of somatostatin-28 (0.2-2.0 nmol) significantly stimulated duodenal bicarbonate secretion in a dose-dependent fashion. Somatostatin-28 was approximately twice as effective as somatostatin-14. Intravenous administration of somatostatin-28 or somatostatin-14 did not significantly alter the bicarbonate response. Ganglionic blockade with chlorisondamine and truncal vagotomy abolished the stimulatory effect of somatostatin-28 while bretylium, naloxone, indomethacin, and adrenalectomy did not. Furthermore, atropine methylnitrate significantly attenuated and the vasoactive intestinal peptide antagonist 4Cl-D-Phe6, Leu17-vasoactive intestinal peptide abolished the bicarbonate response produced by cerebroventricular somatostatin-28. In contrast, hypophysectomy and pretreatment with the vasopressin V1-receptor antagonist [1-deaminopenicillamine, 2-(0-methyl)Tyr, 8-Arg]-vasopressin significantly enhanced the bicarbonate response produced by cerebroventricular somatostatin-28. These findings indicate that somatostatin-28 acts within the central nervous system to stimulate duodenal bicarbonate secretion in freely moving rats via vagal efferents by release of vasoactive intestinal peptide and, in part, by a muscarinic pathway and not by catecholamine, opiate, or prostaglandin release.

Animals↗
PubMed1992

Theophylline and prostaglandin E2 on duodenal bicarbonate secretion: role for 5'-cyclic adenosine monophosphate.

Cyclic adenosine monophosphate (cAMP) has been implicated as an intracellular "second" messenger in duodenal mucosal bicarbonate secretion in animals. The purpose of this study was to determine whether cAMP may mediate duodenal mucosal bicarbonate secretion in humans. In healthy volunteers, a 4-cm segment of proximal duodenum was isolated from gastric and pancreaticobiliary secretions. Either the phosphodiesterase inhibitor theophylline, prostaglandin (PG) E2, or a combination thereof was administered topically to the isolated duodenal mucosa. Theophylline (10(-2) mol/L) and PGE2 (10(-5)-10(-4) mol/L) each significantly increased bicarbonate secretion and transmucosal potential difference. Moreover, when theophylline and PGE2 were administered in combination, the duodenal bicarbonate output was additive compared to either agent alone. When theophylline was infused with increasing doses of PGE2, the dose-response curve was shifted to the left. Furthermore, increases in bicarbonate secretion and transmucosal potential difference were correlated significantly. These results suggest that cAMP may act as an intracellular mediator of human duodenal mucosal bicarbonate secretion.

Adult↗