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PubMed1999

Critical review of the epidemiology literature on the potential cancer risks of methylene chloride.

OBJECTIVE: To critically review and summarize the epidemiological evidence published to date on the carcinogenicity of methylene chloride to humans. METHODS: Papers for review were identified through Medline (National Library of Medicine) and were limited to epidemiology studies. Studies were classified using three categories. Primary studies focused on the association between methylene chloride and cancer among occupational cohorts primarily exposed to methylene chloride. Secondary studies identified methylene chloride a priori as a potential exposure of interest, and the investigators either characterized the methylene chloride exposure or described results for the methylene chloride-exposed workers separately. Tertiary studies evaluated cohorts either minimally exposed to methylene chloride or presumed exposed but for which no exposure estimation or separate classification was made. RESULTS: No strong or consistent finding for any site of cancer was apparent despite several studies of large occupational cohorts of workers potentially exposed to high concentrations of methylene chloride. Sporadic and weak associations were reported for cancers of the pancreas, liver and biliary passages, breast, and brain. Although these studies collectively cannot rule out the possibility of any cancer risk associated with methylene chloride exposure, they do support a conclusion of no substantive cancer risk. CONCLUSIONS: Continued follow-up of the established cohorts may elucidate the few and inconsistent relationships reported to date; however, it appears likely that risks associated with methylene chloride exposure, if any, are small and limited to rare cancers. The usefulness of additional cohort studies for the evaluation of cancer risks associated with methylene chloride exposure will depend largely on whether the relevant exposure period has passed and whether exposure characterization (e.g., peak or intermittent exposure or intensity) can be improved.

Adult↗
PubMed1999

Ultrastructure and distribution dynamics of chloride cells in tilapia larvae in fresh water and sea water.

Integumental and branchial chloride cells of tilapia larvae (Oreochromis mossambicus) were studied at the light-microscopical and ultrastructural level. Total numbers and distribution of chloride cells were quantified after immunostaining of cross sections of the entire larvae with an antibody against the alpha-subunit of Na+/K+-ATPase. The majority (66%) of Na+/K+-ATPase-immunoreactive (ir) cells, i.e. chloride cells, of freshwater tilapia larvae were located extrabranchially up to 48 h after hatching. Five days after hatching, the majority (80%) of chloride cells were found in the buccal cavity. Transfer of 24-h-old larvae to 20% sea water speeded up this process; 24 h after transfer (i.e. 48 h after hatching), the majority (59%) of chloride cells were located in the buccal cavity. The branchial chloride cell population of 24-h- and 120-h-old larvae consisted of immature, mature, apoptotic and necrotic chloride cells. However, relatively more immature chloride cells were observed in freshwater larvae (42-63%) than in (previously studied) freshwater adults (21%), illustrating the developmental state of the gills. After transfer to sea water, the incidence of degenerative chloride cells did not change. Furthermore, the incidence of immature cells had decreased and a new subtype of chloride cells, the "mitochondria-poor" cells, appeared more frequently. These mitochondria-poor chloride cells were characterised by an abundant tubular system and relatively few mitochondria, which were aligned at the border or concentrated in one part of the cytoplasm. Most of these cells did not contact the water. The function of their enhanced appearance after seawater transfer is unknown.

Aging↗
PubMed1987

Mechanism of electroneutral sodium chloride absorption in distal colon of the rat.

This investigation was designed to establish the mechanism of sodium and chloride transport in the rat distal colon by determining ion fluxes across isolated mucosa under voltage clamp conditions. The net rates of sodium and chloride absorption in the distal colon of the rat were approximately equal (5.8 +/- 0.3 and 6.9 +/- 0.5 microEq/h X cm2, respectively) and significantly greater than the short circuit current (0.9 +/- 0.1 microEq/h X cm2). Net sodium absorption and net chloride absorption were markedly reduced by the removal of chloride and sodium, respectively, but were not affected by the absence of potassium from the mucosal bathing solution. Both net sodium absorption and net chloride absorption were also significantly inhibited by 1.0 mM amiloride and by 0.1 mM acetazolamide. In contrast, 0.1 mM amiloride and 1.0 mM furosemide did not inhibit either sodium or chloride absorption. These results confirm that electroneutral sodium chloride absorption is the predominant mechanism of sodium and chloride absorption and suggest that parallel ion (Na-H and Cl-HCO3) exchanges, rather than independent electrogenic sodium and chloride transport, coupled sodium-chloride cotransport, or coupled Na-K-2Cl cotransport, are most likely responsible for sodium chloride absorption in this epithelium.

Acetazolamide↗
PubMed1995

Effect of dietary chloride content on the elimination of bromide by dogs.

The effect of dietary chloride content (0.2, 0.4 and 1.3 per cent chloride on a dry matter basis) on the disposition of a single oral dose of bromide (14 mg kg-1) was evaluated in normal beagles. Increasing the dietary chloride content from 0.2 to 1.3 per cent resulted in a significant decrease in the mean apparent elimination half-life from 69 +/- 22 days to 24 +/- 7 days. The mean area under the concentration curve (AUC) for dogs fed 1.3 per cent chloride was significantly smaller than the AUC for dogs fed 0.2 per cent chloride. Dietary chloride had no effect on the maximum serum concentrations (Cmax) or on the time (Tmax) to reach the maximum concentrations. The steady-state serum bromide concentrations predicted from the single dose data for daily doses of 14 mg kg-1 of bromide were significantly lower in dogs fed 1.3 per cent chloride (310 +/- 150 mg litre-1) than in dogs fed 0.2 per cent chloride (1950 +/- 1140 mg litre-1). The predicted mean daily doses of bromide necessary to maintain serum levels within the therapeutic range for dogs fed 1.3 per cent chloride (43 +/- 13 mg kg-1) were almost twice as high as the dose estimated for dogs fed 0.4 per cent chloride (22 +/- 3 mg kg-1) and nearly three times as high as the dose estimated for dogs fed 0.2 per cent chloride (15 +/- 4 mg kg-1). These differences were statistically significant (P = 0.002).

Animals↗
PubMed1983

Intracellular chloride in retinal neurons: measurement and meaning.

Intracellular chloride activity measurements were obtained from mudpuppy retinal neurons using dual microelectrodes, one of which was made chloride-selective by filling the tip with chloride liquid ion exchange resin. In addition ionic substitution experiments were carried out in the perfused retina-eyecup preparation of the mudpuppy. A comparison of the membrane potential and calculated chloride equilibrium potential shows that retinal neurons differ in relative transmembrane chloride distribution. Ganglion cells have an ECl more negative than the resting membrane potential, whereas amacrine cells have a passive distribution of chloride. Horizontal cells have chloride distributed such that an increase in chloride conductance is depolarizing. On-bipolars have a chloride distribution similar to that of horizontal cells whereas off-bipolars show either passive distribution or some chloride accumulation. These findings are consistent with the idea that chloride ions may play a role as a depolarizing driving force for electrogenic activity of horizontal cells and on-bipolars. Results with Cl substitution experiments are consistent with this interpretation.

Animals↗
PubMed2005

Effect of chloride ions on the oxidation of aniline by Fenton's reagent.

The objective of this study was to experimentally probe the mechanism of chloride ions specifically affecting aniline oxidation by Fenton's reagent. Batch experiments were carried out to investigate the effects of pH, Fe2+, H2O2 and chloride concentration on the oxidation reaction. Results show that the inhibition caused by chloride ions can be overcome by extending the reaction time if the concentration of chloride ions is low. At a high concentration of chloride ions, however, the oxidation of aniline was inhibited, and actually ceased due to the complexation of Fe-Cl. In this study, the chloride ion concentration was kept at 0.2 M in the experiments when studying the effect of ferrous ion concentration on the Fenton reaction. If the ratio of [Cl-]/[Fe2+] was < or = 200, the inhibition effect was very significant. In other words, adding more ferrous ions rather than hydrogen peroxide can break the inhibition originating from the chloride ions at an initial stage of pH 3. The inhibition effect of chloride ions on the aniline reaction depended on the reaction pH; the extent of inhibition decreased with increasing the initial pH as long as the pH was less than 5. Consequently, the inhibition effect by chloride ions was primarily due to the complexation of iron species and chloride ions. The influence of chloride ions on aniline oxidation due to the competition of hydroxyl radicals was not significant.

Aniline Compounds↗
PubMed2002

Effects of Juglans sinensis Dode extract and antioxidant on mercury chloride-induced acute renal failure in rabbits.

This study was undertaken to determine if Juglans sinensis Dode, an oriental medicinal herb, extract (JSE) and antioxidant exert beneficial effect against mercury-induced acute renal failure in rabbits. Acute renal failure was induced by subcutaneous injection of mercury chloride (10 mg/kg), and animals were pretreated with JSE (0.1 g/kg, orally) for 7 days or N,N'-diphenyl-p-phenylenediamine (0.5 g/kg, i.p.) 24 h prior to the injection of mercury chloride. Urine and blood samples were collected for 24 h before (the basal period) and after the administration of mercury chloride. Urine volume and GFR in mercury chloride-injected animals were decreased as compared with the basal values, which were accompanied by the increase in serum creatinine levels and fractional excretion of Na(+), indicating that the administration of mercury chloride produces acute renal failure. p-Aminohippurate uptake by renal cortical slices was inhibited by mercury chloride injection. Mercury chloride treatment in vivo increased lipid peroxidation in renal cortical tissues. Such changes were significantly prevented by JSE pretreatment. Mercury chloride-induced acute renal failure was also prevented by an antioxidant N,N'-diphenyl-p-phenylenediamine. Mercury chloride treatment in vitro increased lactate dehydrogenase release and lipid peroxidation in renal cortical slices, which were prevented by JSE. These results indicate that JSE exerts the beneficial effect against mercury chloride-induced acute renal failure and its effect may be due to antioxidant action. In addition, these results suggest that lipid peroxidation is responsible for the cell injury induced by mercury chloride in vivo and in vitro.

Acute Kidney Injury↗
PubMed1992

Storage in sodium chloride does not impair arterial prostacyclin release.

Heparinised sodium chloride solution is often used for the storage of veins and to prevent clotting in the arterial tree during vascular surgery. Sodium chloride deranges the morphology of endothelial cells and has therefore been interpreted as "toxic" to the endothelial cell. Perfused human saphenous veins and rabbit aortas show the same pattern of prostanoid release even though veins have a lower release than arteries. Excised rabbit aortas were stored in either (a) 0.9% sodium chloride or (b) 0.9% sodium chloride with heparin 5 I.U. ml-1 prior to being mounted in a perfusion model. The vessels were perfused ex vivo for 5 x 15 min with either Hanks' balanced salt solution (HBSS), calcium- and magnesium-free HBSS or 0.9% sodium chloride. For the last period, arachidonic acid (AA) 4 micrograms ml-1 was added. The release of prostacyclin, measured as the stable degradation product 6-keto-PGF1 alpha by radioimmunoassay, was not altered by storage in sodium chloride, or 0.9% sodium chloride plus heparin when compared with control segments. Perfusion with 0.9% sodium chloride did, however, significantly (p greater than 0.05) decrease the prostacyclin production when AA was added. This is most likely to be due to the low pH of the sodium chloride solution. It is concluded that short-term storage of rabbit aorta in sodium chloride plus heparin or 0.9% sodium chloride does not impair the prostacyclin cascade from the vessel wall, which might be of importance when choosing storage medium for reversed veins and veins used for coronary bypass surgery.

6-Ketoprostaglandin F1 alpha↗
PubMed1988

Catalysis of angiotensin I hydrolysis by human angiotensin-converting enzyme: effect of chloride and pH.

The catalysis of the hydrolysis of angiotensin I, an important natural substrate, by human angiotensin-converting enzyme (ACE) was examined in detail as a function of chloride and hydrogen ion concentration. Chloride was found to be a nonessential activator over the pH range 5.0-10.0, with the chloride dependence increasing with increasing pH: the velocity enhancement at optimal [Cl-] increased from 1.6- to 42-fold; the chloride optimum and Ka' increased from 20 to 520 mM and from 0.22 to 120 mM, respectively, and activity in the absence of chloride decreased from 60.9 to 2.4% (relative to maximal activation). Kinetic analyses at pH 6.0, 7.5, and 9.0 confirmed the nonessential activator mechanism. At all pH values tested chloride was found to be inhibitory (relative to maximal activation) at supraoptimal chloride levels. Depending on the [Cl-] range, both apparent uncompetitive and competitive modes were demonstrated. From pH 6.0 to 9.0 Kis varied between 110 and 1140 mM (apparent). In all cases Ki' much greater than Ka'. We suggest that at high [Cl-] chloride binds to low-affinity inhibitory sites on the free enzyme and on the ES and EP complexes. The pH-rate profile demonstrated a chloride-dependent alkaline shift, with the pH optimum increasing from 7.1 at zero chloride to 7.6 at 400 mM NaCl. At [S] much greater than Km a plot of log nu vs pH revealed pKs of 5.9 and 9.4 in the ES complex in the absence of chloride, while at maximally activating [Cl-] only one ionization at pK = 6.3 was observed.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin I↗
PubMed1997

Site-directed mutagenesis of the basic residues 321K to 321G in the CP 47 protein of photosystem II alters the chloride requirement for growth and oxygen-evolving activity in Synechocystis 6803.

CP 47, a component of photosystem II (PSII) in higher plants, algae and cyanobacteria, is encoded by the psbB gene. Site-specific mutagenesis has been used to alter a portion of the psbB gene encoding the large extrinsic loop E of CP 47 in the cyanobacterium Synechocystis 6803. Alteration of a lysine residue occurring at position 321 to glycine produced a strain with altered PSII activity. This strain grew at wild-type rates in complete BG-11 media (480 microM chloride). However, oxygen evolution rates for this mutant in complete media were only 60% of the observed wild-type rates. Quantum yield measurements at low light intensities indicated that the mutant had 66% of the fully functional PSII centers contained in the control strain. The mutant proved to be extremely sensitive to photoinactivation at high light intensities, exhibiting a 3-fold increase in the rate of photoinactivation. When this mutant was grown in media depleted of chloride (30 microM chloride), it lost the ability to grow photoautotrophically while the control strain exhibited a normal rate of growth. The effect of chloride depletion on the growth rate of the mutant was reversed by the addition of 480 microM bromide to the chloride-depleted BG-11 media. In the presence of glucose, the mutant and control strains grew at comparable rates in either chloride-containing or chloride-depleted media. Oxygen evolution rates for the mutant were further depressed (28% of control rates) under chloride-limiting conditions. Addition of bromide restored these rates to those observed under chloride-sufficient conditions. Measurements of the variable fluorescence yield indicated that the mutant assembled fewer functional centers in the absence of chloride. These results indicate that the mutation K321G in CP 47 affects PSII stability and/or assembly under conditions where chloride is limiting.

Base Sequence↗
PubMed1996

Cellular and molecular biology of chloride secretion in the shark rectal gland: regulation by adenosine receptors.

The rectal gland of the dogfish shark (Squalus acanthias) is a sodium chloride secreting epithelial organ whose function was discovered in 1959 by Wendell Burger. The gland, composed of homogenous tubules of a single cell type, is an important model for secondary active chloride transport. Hormonal stimulation of chloride secretion in this system activates asymetrically arranged transport proteins (apical cAMP-activated CFTR-like Cl- channels, basolateral Na/K/2Cl cotransporters, Na/K-ATPase activity, and K+ channels). Five receptors, hormones, and membrane proteins of the shark rectal gland involved in chloride secretion have been cloned recently. Because the intact gland can be perfused via a single artery and vein, it has been possible to examine precisely the metabolic regulation of chloride transport by endogenous adenosine. Rectal gland cells have a high density of both stimulatory A2 type and inhibitory A1 type adenosine receptors. When stimulated by secretagogues, chloride secretion and venous adenosine concentrations increase in parallel, with chloride secretion increasing from approximately 150 to 2100 microEq/hr/g, and adenosine concentrations increasing from approximately 5 to approximately 890 nM. This work of ion transport is accompanied by a marked fall in intracellular ATP activity and a rise in both intracellular AMP and adenosine activity. Agents that prevent the interaction of endogenous adenosine with extracellular receptors significantly increase the chloride transport response to secretagogues. When chloride transport is inhibited by blocking the Na/K/2Cl cotransporter with bumetanide, both adenosine release and chloride secretion fall to basal values. We recently cloned a unique adenosine receptor subtype that is distinct from previously cloned mammalian adenosine receptors. Because of its highly specialized function, single cell type, and simple vascular system, the shark rectal gland is an ideal model system for examining the metabolic regulation of chloride secretion by adenosine receptors.

Animals↗
PubMed1995

Chloride-dependent Na-H exchange. A novel mechanism of sodium transport in colonic crypts.

The mechanism of sodium movement across apical membrane of colonic crypt cells of rat distal colon was examined in studies of both 22Na uptake by apical membrane vesicles (AMV) and the rate of intracellular pH (pHi) recovery from an acid load by the addition of lumen sodium. In the presence of chloride but not in its absence, 22Na uptake in crypt AMV was stimulated by an outward gradient of either [H+] or [Na+]. 22Na uptake stimulated by an outward [Na+] gradient was also observed in the presence of other halides in the order of chloride > bromide > fluoride > iodide. pHi recovery from an acid load was both lumen sodium- and chloride-dependent, and the rate of pHi recovery by lumen sodium in the presence of chloride was 65-fold greater than that in the absence of chloride (dpH/dt is 655.4 and 10.2 in the presence and absence of chloride, respectively). One mM amiloride inhibited both [H+] gradient-stimulated 22Na uptake in the presence of chloride in crypt AMV (80%) and lumen sodium- and chloride-dependent pHi recovery in crypt cells (96%). [H+] gradient stimulation of 22Na uptake by crypt AMV in the presence of chloride was less sensitive to amiloride than amiloride inhibition of Na-H exchange in colonic surface AMV. These studies provide compelling evidence that a chloride-dependent Na-H exchange that is relatively amiloride-resistant is present in the apical membrane of colonic crypt cells. As prior studies have not identified a chloride-dependent Na-H exchange, the molecular and functional basis of this novel transport process is not known.

Amiloride↗
PubMedDate not supplied

Vinyl chloride-a classical industrial toxicant of new interest.

The carcinogenicity of vinyl chloride in humans was recognized in 1974 based on observations of hepatic angiosarcomas in highly exposed workers. A multiplicity of endpoints has been demonstrated. The primary target organ, the liver, displays differential susceptibilities of hepatocytes and sinusoidal cells, which are modified by factors of age and dose. There is consistency in organotropism between experimental animals and humans. Vinyl chloride is a pluripotent carcinogen, predominantly directed toward hepatic endothelial (sinusoidal) cells, and second toward the parenchymal cells of the liver. The similarity of results between experimental animals and humans is a solid basis of an amalgamation of experimental and epidemiological risk estimates. Vinyl chloride requires metabolic activation for carcinogenicity and mutagenicity, and toxicokinetics are a key to interpret the dose response. Practically the entire initial metabolism of vinyl chloride is oxidative. At higher exposure concentrations this is nonlinear, and metabolic saturation of metabolism in rats is reached at about 250 ppm. This is consistent with the plateau of hepatic angiosarcoma incidence in rat bioassays. Physiologically based pharmacokinetic/toxicokinetic (PBPK) models have been developed and successfully applied within the frame of human cancer risk assessments. The major DNA adduct induced by vinyl chloride (approximately 98% of total adducts in rats), 7-(2-oxoethyl)guanine, is almost devoid of promutagenic activity. The clearly promutagenic "etheno" adducts N2,3-ethenoguanine and 3,N4-ethenocytosine each represent approximately 1% of the vinyl chloride DNA adducts in rats, and 1,N6-ethenoadenine is found at even lower concentrations. Etheno adducts appear to have a long persistence and are repaired by glycosylases. Vinyl chloride represents a human carcinogen for which a series of mechanistic events connects exposure with the carcinogenic outcome. These include (1) metabolic activation (to form chloroethylene oxide), (2) DNA binding of the reactive metabolite (to exocyclic etheno adducts), (3) promutagenicity of these adducts, and (4) effects of such mutations on protooncogenes/tumor suppressor genes at the gene and gene product levels. In rat hepatocytes, a further event is a biomarker response. Cancer prestages (enzyme-altered foci), as quantitative biomarkers, provide a tool to study dose response even within low dose ranges where a carcinogenic risk cannot be seen in cancer bioassays directly. Such biomarker responses support a linear nonthreshold extrapolation for low-dose assessment of carcinogenic risks due to vinyl chloride. Published risk estimates based on different sets of data (animal experiments, epidemiological studies) appear basically consistent, and on this basis an angiosarcoma risk of approximately 3 x 10(-4) has been deduced by extrapolation, for exposure to 1 ppm vinyl chloride over an entire human working lifetime. An important point that should be considered in regulatory standard settings is the presence of a physiological background of those etheno DNA adducts, which are also produced by vinyl chloride. Likely reasons for this background are oxidative stress and lipid peroxidation. In essence, fundamentals of the hepatocarcinogenicity of vinyl chloride appear now well established, providing a solid scientific basis for regulatory activities.

Animals↗
PubMed2003

Results of the Massachusetts methylene chloride end-users survey.

A survey of Massachusetts companies reporting use of methylene chloride between 1995 and 1999 was conducted to assess the status of industrial use of the chemical in 2000. Methylene chloride has had wide use in industry although it has been identified as potentially hazardous to exposed workers and the environment. New and tightened occupational and environmental regulations taking effect in the 1990s were hypothesized to have reduced use of the chemical in Massachusetts. Substitute technologies, especially aqueous cleaning, were expected to have replaced methylene chloride in many industries. Seventeen of the 21 Massachusetts manufacturing companies reporting use of over 10,000 lb/y of methylene chloride between 1995 and 1999 were surveyed by telephone regarding their experiences of methylene chloride use and elimination and/or replacement. Fifteen of the 17 companies had either eliminated (10) or reduced to below 10,000 lbs/yr (5) their use of methylene chloride at the time of the survey in 2000. Many of the surveyed companies moved to aqueous cleaning from methylene chloride degreasing operations. Environmental concerns were the most popular reason given for eliminating or reducing use of methylene chloride. Worker health and safety concerns, especially concern about compliance with the 1997 Occupational Safety and Health Administration methylene chloride standard, were also a motivation. In general, the companies associated many benefits and few problems with eliminating or reducing use of methylene chloride. Exposure reduction strategies based on toxics use reduction techniques appear to be feasible for many manufacturing companies. However, research should be conducted to assess the introduction of new hazards as a result of tightened regulations on methylene chloride.

Data Collection↗
PubMed1986

Influence of dietary chloride on fluoride bioavailability in the rat.

A factorial experiment was conducted with weanling rats fed a purified diet to determine the influence of dietary chloride (0.02, 0.10 and 0.50%) as sodium chloride on fluoride bioavailability (2 or 10 ppm as sodium fluoride). After 6 wk, rats fed the lowest chloride-containing diets had significant reductions of plasma chloride, urinary chloride excretion and growth rate compared to other chloride groups. Depressed growth occurred in rats fed chloride-deficient diets despite the fact that food intake was similar for all treatments. Fluoride retention was greatest in chloride-deficient rats, which was reflected in enhanced skeletal uptake of fluoride. Fluoride absorption was not inhibited by high chloride intake. We therefore conclude that emphasis on the effect of chloride on fluoride bioavailability should be directed towards an enhancement of fluoride retention by low salt (sodium chloride) diets rather than in terms of a possible negative effect of a high salt diet on fluoride absorption.

Animals↗
PubMed1993

Chloride anion concentration as a determinant of renal vascular responsiveness to vasoconstrictor agents.

1. The role of chloride concentration in modulating vasoconstrictor responses of the rat isolated kidney, perfused with Krebs-Henseleit solution, to angiotensin II (AII), arginine vasopressin (AVP) and phenylephrine (PE) was investigated. 2. Reduction of perfusate chloride from a high (117 mM) to low (87 mM) concentration, by substitution of sodium chloride with a mixture of sodium salts of propionate, acetate and methanesulphonate, reduced responsiveness to all three vasoconstrictors, the change for AII being most pronounced. 3. For AII, reduced vasoactivity with low chloride was evident both in terms of the threshold dose and on the linear part of the dose-response curve but not for the maximum response. This attenuating effect of low chloride on the vasoconstrictor response to AII was reversed when perfusion with high chloride was reinstituted. Continuous perfusion with high chloride progressively increased the vasoconstrictor effect of low doses of AII for successive dose-response curves. 4. In addition to reducing responses on the linear part of the dose-response curve for both AVP and PE, low chloride also reduced the maximum vasoconstrictor response to PE, whereas the threshold dose for the two agonists was unchanged. In contrast to the enhanced pressor response to AII, during continuous perfusion with high chloride, tachyphylaxis occurred with AVP and PE. 5. The ability of chloride to modify renal responsiveness to vasoconstrictor agents may contribute to the increase in renal vascular resistance and decrease in glomerular filtration rate (GFR) which occurs during infusion of hyperchloremic solutions into the renal artery and explain the need for chloride as the anion accompanying sodium in salt-sensitive hypertensive models.

Angiotensin II↗
PubMed1978

Properties of a conductive cellular chloride pathway in the skin of the toad (Bufo bufo).

Two types of chloride current response to a step-wise hyperpolarization of the toad skin is demonstrated: (1) An "instantaneous" response observed immediately upon voltage change, and (2) a subsequent slow response, the time course of which is sigmoidal. The slow response is due to an increase of a transcellular conductance which is specific to chloride ions. The time constant of the conductance increase is dependent on the amplitude of the transepithelial voltage displacement, the smallest time constants are obtained for the highest amplitudes and are in the order of 30 s. The voltage dependences of the steady-state conductance and the steady-state chloride current reveal that the chloride pathway has maximum conductance for V approximately -80 mV (outside of the skin being negative) and approaches a non-conducting safe for V greater than 0 mV. This strong outward going rectification is a steady-state phenomenon: In skins hyperpolarized for a few minutes, the "instantaneous" I-V curves show that the chloride pathway in the conducting state allows a large inward chloride current (outward chloride flux) to pass in the voltage range 40 mV greater than V greater than 0 mV. Calculations based on a three-compartment model indicate that the strong steady-state chloride current rectification cannot be obtained if only the intracellular chloride concentration and the membrane potentials are allowed to vary ("Goldman-rectification"). It is suggested, therefore, that the premeability of the chloride pathway varies reversibly with the transepithelial potential difference. The variable which controls the chloride permeability may be a membrane potential or the concentration of an intracellular ion.

Amiloride↗
PubMed1972

Temperature dependence of chloride, bromide, iodide, thiocyanate and salicylate transport in human red cells.

1. The temperature dependence of the steady-state self-exchange of chloride between human red cells and a plasma-like electrolyte medium has been studied by measuring the rate of (36)Cl(-) efflux from radioactively labelled cells. Between 0 and 10 degrees C the rate increased by a factor of eight corresponding to an Arrhenius activation energy of 33 kcal/mole.2. The rate of chloride exchange decreased significantly in experiments where 95% of the chloride ions in cells and medium were replaced by other monovalent anions of a lyotropic series. The rate of chloride self-exchange was increasingly reduced by bromide, bicarbonate, nitrate, iodide, thiocyanate, and salicylate. The latter aromatic anion was by far the most potent inhibitor, reducing the rate of chloride self-exchange to 0.2% of the value found in a chloride medium.3. The temperature sensitivity of the chloride self-exchange was not affected significantly by the anionic inhibitors. The Arrhenius activation energies of chloride exchange were between 30 and 40 kcal/mole in the presence of the six inhibitory anions mentioned above.4. The rate of self-exchange of bromide, thiocyanate, and iodide between human red cells and media was determined after washing and labelling cells in media containing 120 mM bromide, thiocyanate, or iodide respectively. The rate of self-exchange of the three anions were 12, 3, and 0.4% of the rate of chloride self-exchange found in the chloride medium.5. The Arrhenius activation energies of the self-exchange of bromide, iodide, and thiocyanate were all between 29 and 37 kcal/mole, the same magnitude as found for the self-exchange of chloride.6. Although approximately 40% of the intracellular iodide and salicylate ions appeared to be adsorbed to intracellular proteins, the rate of tracer anion efflux followed first order kinetics until at least 98% of the intracellular anions had been exchanged.7. The self-exchange of salicylate across the human red cell membrane occurred by a different mechanism than the one utilized by the inorganic monovalent anions. The activation energy of salicylate exchange (13.2 kcal/mole) was significantly lower than that of inorganic anion exchange. Salicylate exchange increased with decreasing pH in contrast to the exchange of chloride, which decreases when pH is lowered.

Adsorption↗