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PubMed1977

Mechanism of active chloride transport by urinary bladder of the Colombian toad.

In order to investigate the mechanism of active chloride transport, experiments were performed to verify the previous report that removal of potassium from the solutions bathing the urinary bladders of Colombian toads induced a reversal of short-circuit current (RSCC) and active chloride transport. The present experiments confirmed these findings. However, there was no correlation between the magnitude of the RSCC and the chloride transport. Furthermore, removal of chloride from the mucosal bathing solutions did not markedly affect the RSCC, indicating that the chloride transport was electrically silent. Removal of bicarbonate from the bathing solutions eliminated the RSCC, and acetazolamide inhibited both the RSCC and net chloride transport. These findings suggest a relationship between chloride and hydrogen ion transport. Inhibition of sodium transport by removal of sodium or addition of ouabain or amiloride has previously been shown to produce an RSCC. In the present experiments these same maneuvers caused an RSCC and induced net chloride transport. It is concluded that active chloride transport by Colombian toad bladder is stimulated by inhibition of sodium transport. The inhibition of active chloride transport by acetazolamide suggests a possible role for carbonic anhydrase in this process.

Acetazolamide↗
PubMed1983

Effect of acute potassium infusion on loop segment chloride reabsorption in the rat.

To assess the effect of acute potassium loading on proximal tubule and loop chloride handling, chloride transport was examined in superficial cortical nephrons in control rats and after infusion with either 0.3 M KNO3 (KVE) or 0.3 M NaNO3 (NaVE) using micropuncture techniques. Infusion with either salt increased plasma volume, single nephron glomerular filtration rate (SNGFR), and delivery of fluid and chloride out of the proximal tubule. Plasma volume, tubule fluid-to-plasma inulin ratio, proximal transepithelial chloride ratio, and absolute and fractional proximal chloride delivery, however, were not different in the NaVE and KVE groups. Early distal tubule fluid flow rate, SNGFR, and fluid reabsorption were greater than control values following either infusion but these were not different between KVE and NaVE. Early distal tubule chloride concentration and transepithelial chloride gradient were greater and fractional chloride reabsorption was less in KVE than in either control or NaVE groups. Calculated fractional loop segment chloride reabsorption was less in KVE animals. These data suggest that potassium loading reduces fractional chloride reabsorption in the loop segment of rat superficial cortical nephrons.

Animals↗
PubMed1984

Mutual dependence of sodium and chloride absorption by renal distal tubule.

Sodium transport and chloride transport by the renal distal tubule of rats were studied by in vivo continuous microperfusion to determine the effects of separately altering luminal sodium and chloride concentrations. Results showed that sodium absorption depends on luminal sodium concentration and chloride absorption depends on luminal chloride concentration; both relations are linear between approximately 10 and 100 mM and have slopes of approximately 2.5 pmol X min-1 X mM-1. Sodium absorption is also a saturable function of luminal chloride concentration, and chloride absorption is a saturable function of luminal sodium concentration; the half-maximal chloride and sodium concentrations are approximately 10 mM. Furosemide, 10(-4) M, when added to the fluid used to perfuse this segment inhibited sodium absorption and chloride absorption to a similar extent. Removal of chloride from luminal fluid (replaced with sulfate) and addition of furosemide to the perfusion fluid had little or no effect on the measured transepithelial voltage. The results are consistent with the presence of a mechanism in the luminal membrane of distal tubule cells that couples the absorptive transport of sodium and chloride.

Absorption↗
PubMed1988

Effect of luminal chloride on cell pH in rabbit proximal tubule.

The present in vitro microperfusion study examined whether apical membrane chloride transport is mediated by chloride-base exchange in the rabbit proximal convoluted (PCT) and proximal straight tubule (PST) by examining the effect of the addition of luminal chloride on intracellular pH. Intracellular pH was measured fluorometrically using the pH-sensitive dye 2',7'-bis(carboxyethyl)-5,6-carboxyfluorescein. In PCT initially perfused without chloride, changing the luminal perfusate to a high chloride (148 mM)-low bicarbonate (5 mM) solution simulating late proximal tubular fluid produced a cell acidification (7.56 +/- 0.06 to 7.52 +/- 0.06, P less than 0.02) when 1 mM formate was present in the perfusate and bathing solution. This acidification was inhibited by 0.5 mM 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid. This chloride-base exchange was not observed in the absence of formate, and neither acetate nor lactate produced the cell acidification observed with formate. Because the Na+-H+ antiporter could blunt a pH change, 2 mM amiloride was added to the luminal perfusate. While addition of luminal chloride produced a small cell acidification in the absence of formate (7.63 +/- 0.06 to 7.60 +/- 0.05, P less than 0.05), a much greater cell acidification was observed in the presence of 1 mM formate (7.69 +/- 0.05 to 7.58 +/- 0.06, P less than 0.01). Chloride-base exchange was only detected in the presence of formate in the PST. These studies demonstrate apical membrane chloride-base exchange in the presence of formate in the rabbit proximal tubule consistent with chloride-formate exchange.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed2005

Effect of short-term supplementation of potassium chloride and potassium citrate on blood pressure in hypertensives.

Randomized trials have shown that increasing potassium intake lowers blood pressure. However, most previous trials used potassium chloride, whereas potassium in fruits and vegetables is not a chloride salt. It is unclear whether a nonchloride salt of potassium has a greater or lesser effect on blood pressure compared with potassium chloride. We performed a randomized crossover trial comparing potassium chloride with potassium citrate (96 mmol/d, each for 1 week) in 14 hypertensive individuals. At baseline, blood pressure was 151+/-16/93+/-7 mm Hg with a 24-hour urinary potassium of 81+/-24 mmol. During the randomized crossover part of the study, blood pressure was 140+/-12/88+/-7 mm Hg with potassium chloride (24-hour urinary potassium: 164+/-36 mmol) and 138+/-12/88+/-6 mm Hg with potassium citrate (24-hour urinary potassium: 160+/-33 mmol). These blood pressures were significantly lower compared with that at baseline; however, there was no significant difference in blood pressure between potassium chloride and potassium citrate, mean difference (95% confidence interval): 1.6 (-2.3 to 5.6) mm Hg for systolic and 0.6 (-2.4 to 3.7) mm Hg for diastolic. Our results, in conjunction with the evidence from many previous trials that potassium chloride has a significant blood pressure-lowering effect, suggest that potassium citrate has a similar effect on blood pressure as potassium chloride. These results support other evidence for an increase in potassium intake and indicate that potassium does not need to be given in the form of chloride to lower blood pressure. Increasing the consumption of foods high in potassium is likely to have the same effect on blood pressure as potassium chloride.

Adult↗
PubMed1985

Synergistic action of cyclic adenosine monophosphate- and calcium-mediated chloride secretion in a colonic epithelial cell line.

Vasoactive intestinal polypeptide (VIP) and the calcium ionophore A23187 caused dose-dependent changes in the potential difference and the short circuit current (Isc) across confluent T84 cell monolayers mounted in modified Ussing chambers. Both VIP and A23187 stimulated net chloride secretion without altering sodium transport. Net chloride secretion accounted for the increase in Isc. When A23187 was tested in combination with VIP, net chloride secretion was significantly greater than predicted from the calculated sum of their individual responses indicating a synergistic effect. VIP increased cellular cyclic AMP (cAMP) production in a dose-dependent manner, whereas A23187 had no effect on cellular cAMP. We then determined whether VIP and A23187 activated different transport pathways. Earlier studies suggest that VIP activates a basolaterally localized, barium-sensitive potassium channel as well as an apically localized chloride conductance pathway. In this study, stimulation of basolateral membrane potassium efflux by A23187 was documented by preloading the monolayers with 86Rb+. Stimulation of potassium efflux by A23187 was additive to the VIP-stimulated potassium efflux. By itself, 0.3 microM A23187 did not alter transepithelial chloride permeability, and its stimulation of basolateral membrane potassium efflux caused only a relatively small amount of chloride secretion. However, in the presence of an increased transepithelial chloride permeability induced by VIP, the effectiveness of A23187 on chloride secretion was greatly augmented. Our studies suggest that cAMP and calcium each activate basolateral potassium channels, but cAMP also activates an apically localized chloride channel. Synergism results from cooperative interaction of potassium channels and the chloride channel.

Calcimycin↗
PubMed2002

Colorimetric determination of chloride in biological samples by using mercuric nitrate and diphenylcarbazone.

A colorimetic method is outlined for the determination of the chloride ion in biological samples (blood serum, plasma, and urine). The present method is based on the quantitative reduction of free mercuric ions by chloride ions. Chloride ions form an indissociable complex with mercuric ions. The remaining free mercuric ions form a purple complex with diphenylcarbazone with an absorption maximum at 550 nm. The reduction of color intensity at 550 nm is directly proportional to chloride concentration in the sample. The linear concentration range in the final reaction mixture was 0-100 microM with a correlation coefficient of -0.9997. The coefficient of variation for the 50 microM chloride ion in the final reaction mixture was 0.9% (n = 6). The analyzed value of chloride concentration in the human control serum Accutrol Normal (Sigma) was 101+/-4 mM (mean+/-SD, n = 12). The certified value of chloride in Accutrol Normal by Sigma is 102 mM, with a mean in the range 91-113 mM. This method was applied to the measurement of urinary chloride excretion in experimental rats. During 16-h urine collection, no food was given and rats had free access to purified water. The urinary excretion rate of chloride was 23.6+/-9.3 micromol/h (mean+/-SD, n = 8) and 126.2+/-28.0 micromol/h (n = 8) for rats fed a normal diet (2.6 g NaCl/kg diet) and a high-salt diet (82.6 g NaCl/kg diet) for 70 d prior to urine collection, respectively. This method is appropriate for low concentrations of chloride in samples or when sample volume is limiting, as in many animal studies such as metabolic urine collection from rats.

Animals↗
PubMedDate not supplied

Active chloride transport powered by Na-K-ATPase in shark rectal gland.

The isolated rectal gland of the spiny dogfish is a unique model for the study of active chloride transport. The gland is stimulated to secrete chloride agains an electrical and a chemical gradient when perfused in vitro by theophylline and/or dibutyryl cyclic AMP. Chloride secretion is depressed by ouabain which inhibits Na-K-ATPase. Thiocyanate and furosemide also inhibit chloride secretion but ethoxolamide, a carbonic anhydrase inhibitor, does not. Chloride transport is highly dependent on sodium concentration in the perfusate. The intracellular concentration of chloride in intact glands exceeds the level expected at electrochemical equilibrium, suggesting active transport of chloride into the cell. These features suggest a general hypothesis for chloride secretion in which the uphill transport of chloride into the cytoplasm is coupled through a membrane carrier to the downhill movement of sodium along its electrochemical gradient. The latter is maintained by the Na-K-ATPase pump while chloride is extruded into the duct by electrical forces.

Animals↗
PubMed1985

The kinetic equation for the chloride transport cycle of band 3. A 35Cl and 37Cl NMR study.

The nature of a transmembrane transport process depends largely on the identity of the reaction that is rate-limiting in the transport cycle. The one-for-one exchange of two chloride ions across the red cell membrane by band 3 can be decomposed into two component reactions: 1) the binding and dissociation of chloride at the transport site, and 2) the translocation of bound chloride across the membrane. The present work utilizes 35 Cl NMR and 37 Cl NMR to set lower limits on the rates of chloride binding and dissociation at the saturated inward- and outward-facing band 3 transport sites (greater than or equal to 10(5) events site-1 s-1 in all cases). At both 0-3 and 37 degrees C, the NMR data specify that chloride binding and dissociation at the saturated transport sites are not rate-limiting, indicating that translocation of bound chloride across the membrane is the slowest step in the overall transport cycle. Using these results, it is now possible to describe many features of the kinetic equation for the ping-pong transport cycle of band 3. This transport cycle can be decomposed into two half-reactions associated with the transport of two chloride ions in opposite directions across the membrane, where each half-reaction is composed of sequential binding, translocation, and dissociation events. One half-reaction contains the rate-limiting translocation event that controls the turnover of the transport cycle; in this half-reaction, translocation must be slower than binding and dissociation. The other half-reaction contains the non-rate-limiting translocation event that in principle could be faster than binding or dissociation. However, when the following sufficient (but not necessary) condition is satisfied, both translocation events are slower than binding and dissociation: if the non-rate-limiting translocation rate is within a factor of 10(2) (0-3 degrees C) or 2 (37 degrees C) of the overall turnover rate, then translocation is rate-limiting in each saturated half-reaction. Thus, even though chloride appears to migrate through a channel that leads from the transport site to solution, the results support a picture in which the binding, dissociation, and channel migration events are rapid compared to the translocation of bound chloride across the membrane. In this case, chloride binding to the transport site can be described by a simple dissociation constant (KD = kappa OFF/kappa ON) rather than by a Michaelis-Menten constant (KM = (kappa OFF + kappa TRANSLOCATION)/KAPPA ON).

Anion Exchange Protein 1, Erythrocyte↗
PubMed1979

Chloride localization in Phaseolus vulgaris leaves exposed to HCl gas.

An investigation of chloride accumulation and distribution in unifoliate leaves of Phaseolus vulgaris following supra-acute exposures to gaseous hydrogen chloride (HCl) was conducted. Plants which were 8-22 days old (post-seeding) were exposed for 20 min to HCl gas in concentrations ranging from 6.0-54.2 mg m-3 in different combinations of age and concentration. Aqueous extracts of treated unifoliates contained more chloride than was present in control leaves. In both 8 and 12-day-old leaves, the amount of chloride accumulated was proportional to the exposure concentration of HCl, but 12-day-old plants accumulated less chloride than 8-day-old plants. The number of leaves with macroscopic injury symptoms (epidermal glazing and interveinal necrosis) was also related to chloride content. Precipitation of chloride ions by silver salts was employed to examine the ultrastructural distribution of chloride. Deposits of AgCl were present in cell walls, ground plasm, vacuoles, and chloroplasts of both control and HCl-treated leaf tissues. In leaves sampled immediately after treatment, chloroplastic AgCl precipitates were less than in controls, but as sampling was delayed from the HCl treatment, AgCl deposits in chloroplasts regained control levels. The frequency and distribution of AgCl deposits indicated that chloride passed through the leaf cuticle and migrated through the apopolast. Chloride also entered the cytoplasm of cells and appeared to be sequestered in vacuoles of treated cells.

Cell Wall↗
PubMed1998

Chloride and sodium transport across bovine ciliary body/epithelium (CBE).

PURPOSE: To study the chloride and sodium ion transports across the bovine ciliary body/epithelium (CBE) by a modified Ussing-Zerahn type chamber. METHODS: Isolated bovine CBE preparations were mounted in a modified Ussing-type chamber and the transepithelial electrical parameters were monitored. The inward (stroma to aqueous) and outward (aqueous to stroma) fluxes of 36[Cl] chloride and 22[Na] sodium ions across the CBE were measured under short-circuited conditions. The effect of 0.1 mM of furosemide and bumetanide on the chloride transport were studied. RESULTS: The potential difference (PD), the resistance and the short-circuit current (SCC) across the isolated bovine ciliary body were found to be -0.20+/-0.01 mV (aqueous negative), 75+/-1 omegacm2 and -2.70+/-0.17 microAcm(-2) (mean+/-SEM, n=50) respectively. A statistically significant net inward chloride ion flux of 1.12+/-0.41 microEq h(-1)cm(-2) (p < 0.01) was found (n=15). The net chloride transport was abolished when 0.1 mM furosemide (82% inhibition) and 0.1 mM bumetanide (100% inhibition) were applied bilateral. No significant net sodium ion flux was detected. CONCLUSIONS: Electrolyte and fluid transport across the bovine CBE may be via a bumetanide and furosemide-sensitive chloride transport mechanism. The Na-K-2Cl cotransporter plays a significant role in the trans-CBE chloride transport. The net chloride flux/current was about 12 times higher than the measured SCC, suggesting that the chloride ion transport may be coupled to other ion species.

Animals↗
PubMedDate not supplied

The contribution of a chloride shunt to the transmucosal potential of the rabbit submaxillary duct.

Chloride movement across the wall of the rabbit submaxillary duct has been studied. It was shown that the chloride diffusion from blood to luminal side was determined primarily by the existing transmucosal potential difference. From the fact that the ouabain-poisoned duct showed symmetrical behavior with respect to the chloride diffusion potentials in both directions and the fact that the measured chloride flux behaved as predicted according to the Goldman equation, it was suggested that a single barrier, rather than a series membrane system, determined the chloride movement. The permeability coefficients for chloride, in the order of 5.5 x 10(-5) cm sce-1 are much larger than would be expected for cell membranes. These findings in combination with the observations that mannitol permeability is higher during chloride perfusion than during sulfate perfusion and the observed electron-microscopic changes favor the concept of the existence of an extracellular route in chloride diffusion. An equivalent electrical circuit is given in order to evaluate the contribution of the chloride shunt more quantitatively. Calculations showed that the ductal resistivity during sulfate perfusion has a value in the order of 434 omega cm2, while during chloride perfusion this value is lowered to 48 omega cm2, indicating that the ductal wall can change from a tight to a leaky epithelium. The implications of these findings are discussed.

Amiloride↗
PubMed1990

Antiplatelet effects of chelerythrine chloride isolated from Zanthoxylum simulans.

Chelerythrine chloride is an antiplatelet agent isolated from Zanthoxylum simulans. Aggregation and ATP release of washed rabbit platelets caused by ADP, arachidonic acid, PAF, collagen, ionophore A23187 and thrombin were inhibited by chelerythrine chloride. Less inhibition was observed in platelet-rich plasma. The thromboxane B2 formation of washed platelets caused by arachidonic acid, collagen, ionophore A23187 and thrombin was decreased by chelerythrine chloride. Phosphoinositides breakdown caused by collagen and PAF was completely inhibited by chelerythrine chloride, while that of thrombin was only partially suppressed. Chelerythrine chloride inhibited the intracellular calcium increase caused by arachidonic acid, PAF, collagen and thrombin in quin-2/AM-loaded platelets. The cyclic AMP level of washed platelets did not elevated by chelerythrine chloride. The antiplatelet effect of chelerythrine chloride was not dependent on the incubation time and the aggregability of platelets inhibited by chelerythrine chloride was easily recovered after sedimenting the platelets by centrifugation and then the platelet pellets were resuspended. Chelerythrine chloride did not cause any platelet lysis, since lactate dehydrogenase activity was not found in the supernatant. These data indicate that the inhibitory effect of chelerythrine chloride on rabbit platelet aggregation and release reaction is due to the inhibition on thromboxane formation and phosphoinositides breakdown.

Adenosine Triphosphate↗
PubMed2005

Phenol chlorination and photochlorination in the presence of chloride ions in homogeneous aqueous solution.

Phenol chlorination was studied in the presence of dissolved Fe(III) and chloride under irradiation and of hydrogen peroxide and chloride in dark acidic solutions. In the former case phenol photochlorination is most likely due to the formation of Cl2*- as a consequence of Fe(III) irradiation in the presence of chloride. The most efficient pathway is the photolysis of FeOH2+ producing hydroxyl, which oxidizes chloride to Cl*. The latter finally yields Cl2*- upon further reaction with chloride. The importance of the pathway involving FeOH2+ is higher at higher pH and moderately low chloride concentration. At pH 2.0 and [Cl-] > 0.03 M chlorophenol generation rate decreases with increasing [Cl-], due to the formation of the much less photoactive species FeCl2+/FeCl2+. The photolysis of FeCl2+/ FeCl2+ yielding Cl* is likely to play an important role at pH 0.5 and high chloride, but under such conditions chlorophenol formation rates are about an order of magnitude lower than at pH 2.0. Due to pH and kinetic constraints, under most environmental conditions the photochemistry of FeCl2+/FeCl2+ can be expected to play a minor role toward chlorination when compared with the one of FeOH2+, which leads to hydroxyl-mediated chloride oxidation. Hydrogen peroxide and chloride react in dark acidic solutions to yield HClO, involved in electrophilic chlorination processes. Chlorophenol formation rates under such conditions are directly proportional to [H+]. The described chlorination and photochlorination processes can take place in acidic aerosols of marine origin, naturally rich in chloride and Fe(III). Antarctic aerosol is also rich of hydrogen peroxide and often strongly acidic due to the presence of sulfuric acid of biogenic origin.

Aerosols↗
PubMed2004

Cyclodextrin effect on solvolysis of substituted benzoyl chlorides.

A kinetic study was carried out on the solvolysis of substituted benzoyl chlorides in the presence of alpha-, beta- and gamma-CD. Combination of the substituent dependent mechanism for solvolysis of benzoyl chlorides and the complexation ability of the cyclodextrin yields the following experimental behavior: (i) catalysis by beta- and gamma-CD for solvolysis of electron-attracting substituted benzoyl chlorides due to the reaction with its hydroxyl group C(6); (ii) absence of alpha-CD influence on solvolysis of benzoyl chlorides with electron withdrawing substituents; (iii) inhibition of solvolysis of benzoyl chlorides with electron-donating groups. This behavior is observed for solvolysis of meta/para substituted substrates in the presence of beta-CD, solvolysis of meta-substituted benzoyl chlorides in the presence of alpha-CD and solvolysis of para-substituted benzoyl chlorides in the presence of gamma-CD. This decrease in the rate constant is a consequence of the complexation of the substrate in the cyclodextrin cavity and its low solvation ability, causing the rate of solvolysis in its interior to be negligible. (iv) The solvolysis of meta-substituted benzoyl chlorides in the presence of gamma-CD yields a new behavior where the reaction of the complexed substrate is not negligible in the interior of the cyclodextrin cavity, which has been interpreted as a consequence of incomplete expulsion of hydration water from its cavity when the complexation takes place. (v) The experimental results obtained in the presence of alpha-CD show that meta-substituted benzoyl chlorides give rise to host : guest complexes with 1 : 1 stoichiometries, whereas those which are para-substituted cause a 2 : 1 stoichiometry to be formed. This difference in behavior has been interpreted taking into account the size of the different benzoyl chlorides and their accommodation in the alpha-CD cavity.

Benzoates↗
PubMed2005

Maturation of rat proximal tubule chloride permeability.

We have previously shown that neonate rabbit tubules have a lower chloride permeability but comparable mannitol permeability compared with adult proximal tubules. The surprising finding of lower chloride permeability in neonate proximals compared with adults impacts net chloride transport in this segment, which reabsorbs 60% of the filtered chloride in adults. However, this maturational difference in chloride permeability may not be applicable to other species. The present in vitro microperfusion study directly examined the chloride and mannitol permeability using in vitro perfused rat proximal tubules during postnatal maturation. Whereas there was no maturational change in mannitol permeability, chloride permeability was 6.3 +/- 1.3 x 10(-5) cm/s in neonate rat proximal convoluted tubule and 16.1 +/- 2.3 x 10(-5) cm/s in adult rat proximal convoluted tubule (P < 0.01). There was also a maturational increase in chloride permeability in the rat proximal straight tubule (5.1 +/- 0.6 x 10(-5) cm/s vs. 9.3 +/- 0.6 x 10(-5) cm/s, P < 0.01). There was no maturational change in bicarbonate-to-chloride permeabilities (P(HCO3)/P(Cl)) in the rat proximal straight tubules (PST) and proximal convoluted tubules (PCT) or in the sodium-to-chloride permeability (P(Na)/P(Cl)) in the proximal straight tubule; however, there was a significant maturational decrease in proximal convoluted tubule P(Na)/P(Cl) with postnatal development (1.31 +/- 0.12 in neonates vs. 0.75 +/- 0.06 in adults, P < 0.001). There was no difference in the transepithelial resistance measured by current injection and cable analysis in the PCT, but there was a maturational decrease in the PST (7.2 +/- 0.8 vs. 4.6 +/- 0.1 ohms x cm2, P < 0.05). These studies demonstrate there are maturational changes in the rat paracellular pathway that impact net NaCl transport during development.

Aging↗
PubMed2000

Separation of chloride and sulfate ions in univalent and divalent cation forms from aqueous streams.

The precipitation and separation of chloride and sulfate in several cation forms (sodium, potassium, magnesium, calcium, strontium, and barium) from aqueous streams were studied using isopropylamine (IPA) and ethylamine (EA) as precipitation solvents. The precipitation fractions (P) of the tested chloride salts at 5000 and 10,000 ppm by both IPA and EA over the studied range of solvents volume ratio (V(R)) were relatively identical (18-60%) and their small variations were within their experimental uncertainty. The P of combined sulfate at 1000 ppm (56-99.5%) and chloride at 5000 ppm (28-62%) in the form of calcium by IPA over the studied range of V(R) were appreciably higher than the P of sulfate (10-98.5%) from calcium sulfate in the absence of calcium chloride, or the P of chloride (18-58%) from calcium chloride in the absence of calcium sulfate. The P of chloride from oil-field-produced waters at 106,654 ppm (20-88%) by both IPA and EA were higher than the P of chloride from diluted produced water at 20,000 (17-68%) and 10,000 ppm (16-65%) over the studied range of V(R). The small amounts of sulfate present in the produced waters (e.g., 435 ppm) were completely removed at V(R) of 0.1 (the first stage of precipitation). Consistency tests performed on the acquired data indicated a good level of experimental consistency. Two model equations (2-Suffix and 3-Suffix) derived from thermodynamic principles of solid-liquid equilibrium (SLE) criteria were employed to correlate the acquired data. While both equations were adequate for correlating the precipitation data, the 3-Suffix equation was more accurate.

Algorithms↗
PubMed1990

Chloride action potentials and currents in embryonic skeletal muscle of the chick.

Chloride-dependent action potentials were elicited from embryonic skeletal muscle fibers of the chick during the last week of in ovo development. The duration of the action potentials was extremely long (greater than 8 sec). The action potentials were reversibly blocked by the stilbene derivative, SITS, a specific blocker of chloride permeability. Using patch clamp pipettes, in which the intracellular chloride concentration was controlled and with other types of ion channels blocked, the membrane potential at the peak of the action potential closely coincided with the chloride equilibrium potential calculated from the Nernst equation. These data indicate that activation of a chloride-selective conductance underlies the long duration action potential. The occurrence of the chloride-dependent action potential was found to increase during embryonic development. The percentage of fibers that displayed the action potential increased from approximately 20% at embryonic day 13 to approximately 70% at hatching. Chloride-dependent action potentials were not found in adult fibers. The voltage and time-dependent currents underlying the action potential were recorded under voltage clamp using the whole-cell version of the patch pipette technique. The reversal potential of the currents was found to shift with the chloride concentration gradient in a manner predicted by the Nernst equation, and the currents were blocked by SITS. These data indicate that chloride ions were the charge carriers. The conductance was activated by depolarization and exhibited very slow activation and deactivation kinetics.

Action Potentials↗