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PubMed1999

Effects of pituitary adenylate cyclase activating polypeptide-27 (PACAP) and vasoactive intestinal polypeptide (VIP) on chloride in HT29 cells studied by X-ray microanalysis.

The colon cancer cell line HT29 is a useful model to study intestinal chloride secretion. These cells have both cAMP-activated and calcium-activated chloride channels. Changes in elemental content of the cells after stimulation with agonists were determined by X-ray microanalysis in the scanning or scanning transmission electron microscope. Exposure of HT29 cells to pituitary adenylate cyclase activating polypeptide-27 (PACAP) caused a transient decrease in the cellular Cl and K concentrations, indicating (net) efflux of chloride. The effect of PACAP is inhibited by somatostatin, which is known to inhibit cAMP-activated as well as calcium-activated chloride secretion and by U-73122, an inhibitor of phospholipase C. Alloxan, an inhibitor of adenylate cyclase, did not significantly affect the PACAP-induced loss of chloride. The calcium-chelating agent EGTA inhibited the PACAP-induced loss of chloride, indicating the need for extracellular calcium ions. Also vasointestinal polypeptide (VIP) caused a decrease of the cellular chloride concentration in HT29 cells. VIP-induced loss of chloride could be inhibited by pre-treating the cells with somatostatin or UK14,304, an alpha-2 adrenergic agonist that has been shown previously to inhibit purinergically activated chloride efflux. Our results indicate that there is cross-talk between the cAMP- and the calcium-activated pathways for chloride secretion in HT29 cells.

Adenylate Cyclase Toxin↗
PubMed1972

Chloride fluxes in isolated dialyzed barnacle muscle fibers.

Chloride outflux and influx has been studied in single isolated muscle fibers from the giant barnacle under constant internal composition by means of a dialysis perfusion technique. Membrane potential was continually recorded. The chloride outfluxes and influxes were 143 and 144 pmoles/cm(2)-sec (mean resting potential: 58 mv, temperature: 22 degrees -24 degrees C) with internal and external chloride concentrations of 30 and 541 mM, respectively. The chloride conductance calculated from tracer measurements using constant field assumptions is about fourfold greater than that calculated from published electrical data. Replacing 97% of the external chloride ions by propionate reduces the chloride efflux by 51%. Nitrate ions applied either to the internal or external surface of the membrane slows the chloride efflux. The external pH dependence of the chloride efflux follows the external pH dependence of the membrane conductance, in the range pH 3.9-4.7, increasing with decreasing pH. In the range pH 5-9, the chloride efflux increased with increasing pH, in a manner similar to that observed in frog muscle fibers. The titration curve for internal pH changes in the range 4.0-7.0 was quantitatively much different from that for external pH change, indicating significant asymmetry in the internal and external pH dependence of the chloride efflux.

Animals↗
PubMed1985

Renin secretion and loop of Henle chloride reabsorption in the adrenalectomized rat.

Renin release is increased in the adrenalectomized rat and is not inhibited by sodium chloride administration. The purpose of this study was to determine whether increased renin release is related to impaired absorptive chloride transport in the loop of Henle. Chloride transport in the loop was measured before and after acute saline infusion in three groups of rats: 1) saline-drinking adrenalectomized rats (Adx); 2) saline-drinking dexamethasone-treated adrenalectomized rats (Dex); and 3) water-drinking sham-operated controls. Unrelated to differences of arterial pressure, glomerular filtration rate, or net sodium chloride balance, chloride reabsorption in the loop of Henle of Adx [836 +/- 172 peq/min (SE)] was less (P less than 0.01) than in controls (1,646 +/- 353) and Dex (1,377 +/- 318) before saline infusion. After saline infusion, chloride delivery to the loop increased (P less than 0.05) in all three groups. However, loop chloride reabsorption increased (P less than 0.01) only in controls and Dex but not in Adx. Before saline infusion, plasma renin concentration (PRC) of Adx (350 +/- 108 U/ml) was greater (P less than 0.01) than that in controls (56 +/- 6) or Dex (108 +/- 36); sodium chloride infusion failed to inhibit PRC in Adx, whereas PRC was suppressed (P less than 0.01) by saline in Dex and controls. Thus stimulation of renin release in adrenalectomized animals was associated with decreased absorptive chloride transport in the loop of Henle. Dexamethasone normalized loop function and renin responsiveness to sodium chloride.

Absorption↗
PubMed1986

Effect of dietary NaCl on chloride uptake in rat collecting duct segment.

To explore further the mechanism of the effect of dietary NaCl intake on collecting duct (CDS) chloride uptake, we compared late distal chloride delivery to and urinary 36Cl recovery (the latter as an index of unidirectional efflux) from the CDS in four groups of male Sprague-Dawley rats. Groups were prepared for 7-10 days as follows: group 1, drinking 0.15 M NaCl; group 2A, regular diet; group 2B, regular diet plus deoxycorticosterone (2 mg im) (at 24 and 2 h before micropuncture); and group 3, low-NaCl diet. To increase tubule fluid flow rate and produce natriuresis without chloruresis, 0.15 M NaHCO3 at 5% body wt/h was infused in all groups except group 3, in which an infusion of 150 mM Na+, 55 mM Cl-, and 85 mM HCO3- was required to maintain a plasma chloride concentration equal to that in other groups. Plasma chloride concentration and arterial pH did not differ between groups before infusion. Urinary 36Cl recovery increased in parallel with dietary NaCl content (P = 0.0001). By analysis of multiple covariances, neither tubule fluid chloride concentration nor chloride delivery to the CDS correlated with urinary 36Cl recovery within any of the groups or for all animals studied. High doses of mineralocorticoid did not alter chloride uptake in group 2. These data suggest that progressive restriction of dietary NaCl enhances chloride uptake in the CDS of the rat unrelated to changes in plasma chloride concentration or chloride delivery from the superficial late distal tubules.

Animals↗
PubMed1998

Effect of diuretics on sodium and chloride permeability in the rat papillary collecting duct.

While in vivo data suggests that diuretics such as furosemide and hydrochlorothiazide alter inner medulla collecting duct (IMCD) cell electrolyte transport, this has not been confirmed by in vivo studies nor have the mechanisms been evaluated. This study evaluated the direct effect of these diuretics as well as amiloride on sodium and chloride unidirectional permeability in the isolated perfused rat IMCD. In the absence of diuretics, the permeability of sodium was lower than that of chloride (0.63 +/- 0.05 compared with 0.83 +/- 0.08 micrometer/s), although both were relatively impermeable when compared to water. Furosemide (10(-4)) and hydrochlorothiazide (10(-3)) both increased the diffusional permeability of chloride by approximately 30% (0.80 +/- 0.06 to 1.04 +/- 0.09 micrometer/s, p < 0.01, and 0.74 +/- 0.09 to 0.98 +/- 0.10 micrometer/s, p < 0.02, respectively). However, sodium permeability was unaltered. Inhibition of Na+, K+-ATPase by ouabain or cooling (4 degrees C) inhibited basal sodium but not chloride permeability while a maximal antidiuretic AVP concentration did not alter sodium or chloride permeability. However, increasing the lumen and bath sodium chloride concentration from 150 to 300 and 600 mM significantly increased both sodium and particularly chloride conductance. In contrast, amiloride (10(-4)) significantly reduced both sodium and chloride permeability. These studies support a direct effect of furosemide and hydrochlorothiazide on the IMCD and suggest that their in vivo effect is primarily mediated by facilitating the passive movement of chloride into the lumen via a favourable electrochemical gradient. These results also demonstrate that amiloride inhibits both sodium and chloride unidirectional permeability by mechanisms separate to that of the sulphonamide-related diuretics.

Amiloride↗
PubMed2000

Atrial natriuretic factor binding to its receptor is dependent on chloride concentration: A possible feedback-control mechanism in renal salt regulation.

Although considerable evidence indicates a role for atrial natriuretic factor (ANF) in renal salt regulation, other studies have found a lack of natriuretic response to high-plasma ANF under certain physiological and pathophysiological conditions. The mechanism for this apparent insensitivity to ANF is unknown. In the present study, it was found that ANF binding to its receptor requires the presence of chloride and occurs in a chloride concentration-dependent manner. ANF binding was measured using the purified recombinant hormone-binding domain of the ANF receptor in the presence of 0.1 mol/L NaCl or other selected salt. High specific binding was detected in the presence of NaCl, KCl, or NH(4)Cl. However, binding was undetectable when the salt was replaced with NaHCO(3), CH(3)COONa, or CH(3)COONH(4), indicating that binding requires the presence of chloride. Chloride dependence was also found with the native receptor in bovine adrenocortical membrane preparations. ANF binding to the recombinant protein was chloride concentration-dependent over a range from 0.05 to 10 mmol/L, and a half-maximum binding was attained at approximately 0.6 mmol/L equivalent chloride concentration. Competitive-binding assays at several fixed concentrations of NaCl showed that lowering chloride concentration caused a decrease in maximum binding but did not alter K(d) values, suggesting that a loss of chloride turns off ANF binding rather than reducing affinity for ANF. Saturation-binding studies showed that excess ANF cannot overcome loss of binding caused by low chloride. Chloride-dependent ANF-receptor binding may function as a feedback-control mechanism regulating the ANF-receptor action and, hence, renal sodium excretion.

Animals↗
PubMed2003

Influence of salinity on the localization of Na+/K+-ATPase, Na+/K+/2Cl- cotransporter (NKCC) and CFTR anion channel in chloride cells of the Hawaiian goby (Stenogobius hawaiiensis).

Na+/K+-ATPase, Na+/K+/2Cl- cotransporter (NKCC) and cystic fibrosis transmembrane conductance regulator (CFTR) are the three major transport proteins thought to be involved in chloride secretion in teleost fish. If this is the case, the levels of these transporters should be high in chloride cells of seawater-acclimated fish. We therefore examined the influence of salinity on immunolocalization of Na+/K+-ATPase, NKCC and CFTR in the gills of the Hawaiian goby (Stenogobius hawaiiensis). Fish were acclimated to freshwater and 20 per thousand and 30 per thousand seawater for 10 days. Na+/K+-ATPase and NKCC were localized specifically to chloride cells and stained throughout most of the cell except for the nucleus and the most apical region, indicating a basolateral/tubular distribution. All Na+/K+-ATPase-positive chloride cells were also positive for NKCC in all salinities. Salinity caused a slight increase in chloride cell number and size and a slight decrease in staining intensity for Na+/K+-ATPase and NKCC, but the basic pattern of localization was not altered. Gill Na+/K+-ATPase activity was also not affected by salinity. CFTR was localized to the apical surface of chloride cells, and only cells staining positive for Na+/K+-ATPase were CFTR-positive. CFTR-positive cells greatly increased in number (5-fold), area stained (53%) and intensity (29%) after seawater acclimation. In freshwater, CFTR immunoreactivity was light and occurred over a broad apical surface on chloride cells, whereas in seawater there was intense immunoreactivity around the apical pit (which was often punctate in appearance) and a light subapical staining. The results indicate that Na+/K+-ATPase, NKCC and CFTR are all present in chloride cells and support current models that all three are responsible for chloride secretion by chloride cells of teleost fish.

Analysis of Variance↗
PubMed1995

Chloride transport activation by plasma osmolarity during rapid adaptation to high salinity of Fundulus heteroclitus.

Transition from low salt water to sea water of the euryhaline fish, Fundulus heteroclitus, involves a rapid signal that induces salt secretion by the gill chloride cells. An increase of 65 mOsm in plasma osmolarity was found during the transition. The isolated, chloride-cell-rich opercular epithelium of sea-water-adapted Fundulus exposed to 50 mOsm mannitol on the basolateral side showed a 100% increase in chloride secretion, which was inhibited by bumetanide 10(-4) M and 10(-4) M DPC (N-Phenylanthranilic acid). No effect of these drugs was found on apical side exposure. A Na+/H+ exchanger, demonstrated by NH4Cl exposure, was inhibited by amiloride and its analogues and stimulated by IBMX, phorbol esters, and epithelial growth factor (EGF). Inhibition of the Na+/H+ exchanger blocks the chloride secretion increase due to basolateral hypertonicity. A Cl-/HCO3- exchanger was also found in the chloride cells, inhibited by 10(-4) M DIDS but not involved in the hyperosmotic response. Ca2+ concentration in the medium was critical for the stimulation of Cl- secretion to occur. Chloride cell volume shrinks in response to hypertonicity of the basolateral side in sea-water-adapted operculi; no effect was found on the apical side. Fresh-water-adapted fish chloride cells show increased water permeability of the apical side. It is concluded that the rapid signal for adaptation to higher salinities is an increased tonicity of the plasma that induces chloride cell shrinkage, increased chloride secretion with activation of the Na+K+2Cl- cotransporter, the Na+/H+ exchanger and opening of Cl- channels.

Adaptation, Physiological↗
PubMed2006

Role of chloride transport proteins in the vasorelaxant action of nitroprusside in isolated rat aorta.

Chloride ions play a key role in smooth muscle contraction, but little is known concerning their role in smooth muscle relaxation. Here we investigated the effect of chloride transport inhibitors on the vasorelaxant responses to nitroprusside in isolated and endothelium-denuded rat aorta, precontracted with phenylephrine 1 muM. Incubation of aortic rings in NO(3)(-) media strongly potentiated the vasorelaxant responses to nitroprusside. Bumetanide, DIDS (4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid) and acetazolamide strongly potentiated the vasorelaxant responses to nitroprusside (by 70-100%). EC(50) were 2.3+/-0.5 microM for bumetanide, 26+/-15 microM for DIDS and 510+/-118 microM for acetazolamide (n=6 for condition). Niflumic acid, a selective inhibitor of ClCa (calcium-activated chloride channels), potentiated nitroprusside relaxation to a similar extent as chloride transport inhibitors, in a non-additive manner. Zinc and nickel ions, both modestly potentiated nitroprusside vasorelaxation (by 20-30%). Cobaltum had negligible effect on nitroprusside vasorelaxation. CPA (p-chlorophenoxy-acetic acid), an inhibitor of volume-sensitive chloride channels (ClC), slightly potentiated nitroprusside vasorelaxation (by 15%), and the cystic fibrosis transmembrane conductance regulator (CFTR) chloride channel inhibitors CFTR(inh)172 (5-[(4-Carboxyphenyl)methylene]-2-thioxo-3-[(3-trifluoromethyl)phenyl-4-thiazolidinone), DPC (diphenylamine-2,2'-dicarboxylic acid) and glibenclamide were without significant effect. In conclusion, inhibition of chloride transport proteins strongly potentiates the vasorelaxant responses to nitroprusside in isolated rat aorta. This effect seems mediated by chloride depletion and inhibition of a chloride channel activated by both, calcium and cyclic GMP (cGMP).

Animals↗
PubMed2006

Removal of terephthalic acid in alkalized wastewater by ferric chloride.

Terephthalic acid, which is a main component in alkali-decrement wastewater, is efficiently removed using ferric chloride in high pH solutions. About 90% removal of terephthalic acid is achieved at pH between 8 and 11. Especially, the removal reached 94.3% at pH 11. However, as the pH increased from pH 12 and 13, the low removal of terephthalic acid were found. The increasing ferric chloride dosage had a dramatic positive impact on the achieved removal of terephthalic acid. Further increase in the ferric chloride dosage did not produce better removal rate. The increase of terephthalic acid concentration also led to the increase of ferric chloride dosage in order to get the same removal of terephthalic acid. There was approximately a negative linear relationship between terephthalic acid concentration and removal of terephthalic acid. Compared with other coagulants, it can be seen that ferric chloride is more effective in a high pH solution and the amount of ferric chloride required is also less as compared with aluminum chloride, magnesium chloride and calcium chloride. Our results clearly showed that terephthalate anions strongly binds to positive Fe(OH)(3) flocs and forms insoluble complexes, probably through a mechanism involving electrostatic attraction. The electrostatic attraction may be particularly useful means of purifying wastewater in high pH solutions.

Adsorption↗
PubMed2006

Use of sodium concentration and anion gap to improve correlation between serum chloride and bicarbonate concentrations.

Although most acid-base disorders cause opposite and equal changes in serum chloride and bicarbonate concentrations, this inverse relationship can be distorted by changes in the anion gap and/or water balance. Therefore, we examined the relationship between chloride and bicarbonate before and after adjusting for anion gap and serum sodium concentration. Patients with abnormal electrolytes were grouped by chloride and bicarbonate concentrations (low, normal, and high). Then, chloride and anion gap-adjusted bicarbonate were adjusted for water excess (or deficit), manifesting as hyponatremia (or hypernatremia), after which patients were reclassified. Classification by chloride and bicarbonate changed in 82% of the 135 patients after adjustment for anion gap and sodium. Serum chloride and bicarbonate were each low (concordant) in 23 patients, while 18 had discordant chlorides and bicarbonates (9 low/high, 9 high/low). After adjustments, chloride and bicarbonate were discordant in 40 patients (31 low/high, 9 high/low) and concordant in none. The correlation between serum chloride and bicarbonate improved from -0.459 to -0.998 after adjustments for sodium and anion gap. A very close inverse relationship between serum chloride and bicarbonate concentrations is commonly distorted by concomitant water disturbances and anion gap acidoses in internal medicine patients admitted with electrolyte disorders.

Acid-Base Equilibrium↗
PubMed1978

Asymmetry of the chloride transport system in human erythrocyte ghosts.

The concentration dependence of the unidirectional chloride flux and the inhibition of the unidirectional chloride flux by sulfate were studied in human red cell ghosts. The concentration dependence of the unidirectional chloride flux and its inhibition by sulfate were asymmetric. The unidirectional chloride flux can be saturated from the inner and from the outer membrane surface. For the inner membrane surface, lower chloride half-saturation constants were obtained than for the outer membrane surface. The inhibition of the unidirectional chloride flux by sulfate is competitive. In contrast to the chloride half-saturation constants, the inhibition constants of sulfate for the inner membrane surface were higher than the inhibition constants of sulfate for the outher membrane surface. Either there are fixed anion binding sites at the inner and at the outer membrane surface which control the access of anions to a pore, or there is a mobile carrier which is in contact with both membrane surfaces. The asymmetry of the concentration response and of the inhibition of the unidirectional chloride flux suggest that the anion binding sites at the inner and at the outer membrane surface differ with respect to their affinities for chloride and for sulfate. Alternatively, the asymmetry of the chloride transport system could indicate an asymmetric distribution of a mobile anion carrier across the erythrocyte membrane.

Anions↗
PubMed1985

Chloride transport across the integumentary epithelium of Manduca sexta (Lepidoptera: Sphingidae).

Moulting fluid of Manduca sexta contains high concentrations of potassium and bicarbonate (100 mM) and low concentrations of chloride (5 mM). This fluid begins to disappear from the exuvial space approximately 9-10 h before the actual shedding of the integument. During this time, the integument can be isolated in an Ussing cell and electrical properties measured in vitro. In a normal 32 mM KHCO3 saline, potential difference (PD) is around 10 mV, exuvial side positive, and short-circuit current (SCC) is 15-20 microA cm-2. Substitution of chloride slightly reduces both PD and SCC, although resistance does not change significantly. Measurement of chloride transport in the absence of K+ indicates that 100% of the SCC can be accounted for by the net chloride flux (approximately 2 microA cm-2). The Km and Jmax for transepithelial chloride transport are 14 mM and 0.1 microEq cm-2 h-1. Bilateral potassium addition stimulates chloride transport, doubling net chloride flux as potassium concentration increases from 2 to 5 mM. Chloride net flux is not inhibited by the presence of furosemide (1 mM), nor in HCO3- -free saline by thiocyanate (1 or 10 mM) or acetazolamide (0.1 mM), but is inhibited by 100% N2. The pattern of chloride transport in M. sexta is similar to that previously reported for the rectum of locusts. As chloride is normally at low concentrations in the moulting fluid, it is suggested that this transport system acts to maintain low intracellular concentrations which may be necessary for enzymatic functions in the epidermal cells and has little importance in fluid transport.

Animals↗
PubMed2001

Chloride distribution in the CA1 region of newborn and adult hippocampus by light microscopic histochemistry.

GABA, the main inhibitory neurotransmitter in the central nervous system, exerts its effect by rendering the postsynaptic GABAA receptors permeable to chloride ions. Thus, depolarizing or excitatory effects of GABA, experienced in early postnatal life or in certain regions and/or conditions of the adult brain, is thought to be associated with a reversed transmembrane chloride gradient. However, there is only limited direct information about the correlation of the actual excitatory versus inhibitory effects of GABA and the local chloride distribution. Precipitation of chloride with silver is a potential way to immobilize and visualize chloride ions in biological tissue. We examined the applicability of light microscopic histochemistry, based on trapping tissue chloride with silver ions during freeze-substitution or aldehyde fixation, to visualize the chloride distribution in hippocampal slices. The freeze-substitution procedure yielded better chloride retention while with aldehyde fixation tissue preservation was more appropriate. Both methods were qualitative only, had limited applicability to the superficial 20-30 microns of slices, but were able to demonstrate a reduced extracellular-to-intracellular chloride gradient in the CA1 pyramidal neurons of the newborn hippocampus as compared to adult animals. In the 4-aminopyridine model of epilepsy, redistribution of chloride from extracellular to intracellular space could also be demonstrated.

4-Aminopyridine↗
PubMed1998

Acetylcholine-activated chloride current in the T-84 colonic cell line.

The stimulation of epithelial chloride secretion by hormones and neurotransmitters involves the activation of apical membrane chloride channels. The regulation of chloride current by acetylcholine in the T-84 colonic cell line was investigated using single-channel patch-clamp techniques. Treatment with carbachol resulted in the stimulation of transient chloride currents in 18 of 32 previously quiescent patches. Lack of resolvable single-channel openings suggests that single-channel conductance is less than 5-pS. Of 18 responsive patches, 4 showed multiple current oscillations. Treatment of the cells with AlF4- activated sustained chloride currents, suggesting that G proteins are involved. In excised patches, chloride current was markedly sensitive to free Ca2+ concentrations between 500 and 1000 nM. Time-dependent activation and inactivation of chloride current occurred at +60 and -60 mV. These results indicate that the chloride channels responsible for cholinergic activation of chloride conductance in the T-84 colonic cell line are members of the very low conductance family of chloride channels.

Acetylcholine↗
PubMed1990

Chloride-dependence of amino acid transport in rabbit ileum.

Chloride-dependence of influx across the brush-border membrane of distal rabbit ileum was examined for beta-alanine, 2-methylaminoisobutyric acid (MeAIB), leucine, lysine, proline and D-glucose. Influx of leucine at 2 mM and of D-glucose at 0.5 mM was chloride-independent indicating that substitution of isethionate for chloride has no unspecific effect on sodium gradient driven transport processes. In contrast influx of beta-alanine and MeAIB was totally dependent on the presence of chloride ions. In the absence of chloride, proline transport was reduced to 20% of its control level. This remaining transport can be accounted for by the function of the carrier of alpha-amino-monocarboxylic acids. Transport of leucine at 0.1 mM was reduced by absence of chloride. This is in accordance with the observation of leucine transport by the beta-alanine carrier. The kinetics of chloride and sodium activation of transport of MeAIB were examined at 1 mM MeAIB. Chloride activation was characterized by a Hill coefficient of 1 and a K1/2 of 23.5 mM, and sodium activation by a Hill coefficient of 2 and a K1/2 of 51 mM. Thus cotransport of chloride with an imino acid would be compatible with the known rheogenic nature of this transport. This study adds the imino acid carrier and the beta-alanine carrier to the group of chloride-dependent, epithelial amino acid transport systems.

Amino Acids↗
PubMed1985

Attenuation of murine coronavirus infection by ammonium chloride.

Ammonium chloride at a concentration of 20 mM delayed by 4-5 hr the production of virus progeny in mouse L-2 cells infected at high multiplicity with mouse hepatitis virus (MHV). This delay was seen in the production of both intracellular and extracellular virus. However, the final titers were similar to those produced by MHV-infected cells maintained in normal medium. The manifestation of virus-induced cell fusion was similarly found to be delayed, but not otherwise decreased in severity, when ammonium chloride was present in the culture medium. Ammonium chloride caused similar delays in production of virus-specific, positive-sense RNAs and of viral polypeptides. The relative proportions and apparent molecular weights of viral RNAs and polypeptides were similar to those found in MHV-infected cells cultured in normal medium. In vitro translation of endogenously produced viral RNAs in cell extracts, prepared from MHV-infected cells, was not inhibited by ammonium chloride. Thus, ammonium chloride has no specific, inhibitory effect on viral protein synthesis. Ammonium chloride did not reduce the number of virus-infected cells in culture, as monitored by infectious center assay. Analysis of early events in MHV infection showed that ammonium chloride did not affect adsorption or internalization of MHV by L-2 cells. However, the subsequent eclipse phase, as monitored by decline in infectivity of internalized virus inoculum proceeded less efficiently in the presence of ammonium chloride. On the basis of the known inhibitory effects of ammonium chloride on lysosomal/endosomal functions, the results suggest an endosomal mechanism of MHV uncoating. Thus the primary effect of ammonium chloride on MHV infection of L-2 cells is to attenuate virus uncoating, thereby chronologically displacing all subsequent virus-encoded functions.

Ammonium Chloride↗
PubMed1995

Chloride-dependent amino acid transport in the small intestine: occurrence and significance.

The unidirectional influx of amino acids, D-glucose and ions across the brush-border membrane of the small intestine of different species has been measured in vitro with emphasis on characterization of topographic and species differences and on chloride dependence. The regional differences in transport along the small intestine are outlined and shown to be caused by variation in transport capacity, while the apparent affinity constants are unchanged. Rabbit small intestine is unique by exhibiting maximal rates of transport in the distal ileum and a very steep decline in the oral direction from where tissues are normally harvested for preparation of brush-border membrane vesicles. Transport in the guinea pig and rat is much more constant throughout the small intestine. Since the capacity of nutrient carriers is regulated by their substrates it is possible that bacterial breakdown of peptides and proteins in rabbit distal ileum increases the concentration of amino acids leading to an upregulation of the carriers. Chloride dependence is a characteristics of the carrier rather than the transported amino acid, and is used to improve the classification of amino acid carriers in rabbit small intestine. In this species the imino acid carrier, the beta-amino acid carrier, and the beta-alanine carrier, which should be renamed the B0,+ carrier, are chloride-dependent. The steady-state mucosal uptake of classical substrates for these carriers in biopsies from the human duodenum is also chloride-dependent. The carrier of beta-amino acids emerges as ubiquitous and chloride-dependent, and evidence of cotransport with both sodium and chloride is reviewed. A sodium:chloride:2-methyl-aminoisobutyric acid coupling stoichiometry of approx. 2:1:1 is suggested by ion activation studies. Direct measurements of coupled ion fluxes in rabbit distal ileum confirm that sodium, chloride and 2-methyl-aminoisobutyric acid are cotransported on the imino acid carrier with an identical influx stoichiometry. Control experiments and reference to the literature on the electrophysiology of the small intestine exclude alterations of the membrane potential as a feasible explanation of the chloride dependence. Thus, it is concluded that chloride is cotransported with both sodium and 2-methyl-aminoisobutyric acid across the brush-border membrane of rabbit distal ileum.

Amino Acids↗