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PubMed1986

Studies on the inhibition of brain synaptosomal Na+/K+-ATPase by mercury chloride and methyl mercury chloride.

The effect of mercury chloride (HgCl2) and methyl mercury chloride (MeHg) on brain synaptosomal Na+/K+-ATPase was determined in vitro. It was shown that HgCl2 is a more powerful inhibitor than MeHg. The IC50 were 5 X 10(-7) M for HgCl2 and 2.3 X 10(-6) M for MeHg. A non-competitive type of inhibition was observed with the two mercurials. Removal of contaminating lipids with the non-ionic detergent Lubrol did not affect the inhibition of either mercurial. It is concluded that non-essential lipids do not play a significant role in the inhibitory effect of MeHg and that the potency of these mercurials on to inhibit brain synaptosomal Na+/K+-ATPase largely depends on their capacity to block sulfhydryl groups.

Animals↗
PubMed1990

Zinc inhibition of chloride efflux from skeletal muscle of Rana pipiens and its modification by external pH and chloride activity.

Efflux of 36Cl- from frog sartorius muscles equilibrated in depolarizing solutions was measured. Cl- efflux consists of a component present at low pH and a pH-dependent component which increases as external pH increases. In depolarized muscles from Rana pipiens, the pH-dependent Cl- efflux has an apparent pKa near 6.4. The reduction of Cl- efflux by external Zn2+ was determined at different external pHs and chloride activities. The effect of external chloride activity on the pH-dependent Cl- efflux was also examined. At pH 6.5 and a membrane potential of -22 mV, increasing external Cl- activity from 0.108 to 0.28 M decreased inhibition of the pH-dependent Cl- efflux at all activities of Zn2+. The Zn2+ activity needed to reduce Cl- efflux by half increased from 0.39 x 10(-3) to 2.09 x 10(-3) M. By contrast, external Cl- activity had no measurable effect on the apparent pKa of the pH-dependent efflux. At constant Cl- activity less than 0.21 M, increasing external pH from 6.5 to 7.5 decreased inhibition by low Zn2+ activities with either a slight increase or no change in the Zn2+ activity producing half-inhibition. In other words, for relatively low Cl- activities, protection against inhibition of Cl- efflux by low Zn2+ activities was obtained by raising, not lowering, external pH; this is not what is expected if H+ and Zn2+ ions compete at the same site to produce inhibition of Cl- efflux. We conclude that Zn2+ and low pH inhibit Cl- efflux by separate and distinct mechanisms.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

Effects of light and inhibitors of ATP-synthesis on the chloride carrier of the alga Valonia utricularis: is the carrier a chloride pump?

The effect of metabolic inhibitors, such as cyanide, antimycin A and azide was studied on the chloride transport system of the giant marine alga Valonia utricularis by using the charge pulse relaxation method. Two clearly defined voltage relaxations were resolved. The addition of 10-30 microM cyanide to the artificial sea water (ASW) bathing the algal cells increased the time constants of the slow voltage relaxation, tau 2, significantly when the algal cells were kept in the dark. The cyanide-effect reached a plateau value at 100-300 microM and was fully reversible when cyanide was removed from the ASW. Analysis of the charge pulse data in terms of the Läuger-model demonstrated that the translocation rates of the free, kS, and the charged carrier, kAS, decreased. The decrease of kS was more pronounced than that of kAS. 10 microM antimycin A and 3 mM azide had similar effects on the rate constants when the light was switched off. Upon illumination the cyanide- and antimycin A-, but not the azide-mediated effects disappeared. At concentrations higher than 1 mM cyanide caused a further, dramatic decrease of kS and kAS, while the surface concentration of the carrier molecules, N0, was not affected. This cyanide-effect was also reversible, but not light-dependent. Measurements of the ATP level showed that 3 mM cyanide reduced the ATP level by about 70% both under light and dark conditions. In the presence of 30 microM cyanide (or 10 microM antimycin A) the ATP level decreased by about 50%, but only in the dark. These results suggest two different effects of cyanide on the Cl(-)-carrier system: in the micromolar concentration range cyanide (and antimycin A) reduced predominantly the translocation of the free carrier by inhibition of ATP synthesis by oxidative phosphorylation, whereas in the millimolar concentration range cyanide apparently inhibits the translocation rates of both the free and charged carriers by its binding to the carrier. The results provide some evidence that the chloride transport of V. utricularis could be coupled to metabolic energy but it is an open question whether it is a pump or not.

Adenosine Triphosphate↗
PubMed1984

The comparative effects of methylmercuric chloride and mercuric chloride upon DNA synthesis in mouse fetal astrocytes in vitro.

The relative effects of direct exposure to methylmercuric chloride (MMC) and mercuric chloride (MC) upon [3H]thymidine incorporation were determined using cultured mouse fetal astrocytes. The labeling indices of cells exposed to MMC were significantly lower than those of cells exposed to equimolar concentrations of MC. These results indicate that on a mole-for-mole basis, MMC is much more deleterious upon DNA synthesis of mouse fetal astrocytes than those of MC.

Animals↗
PubMed1990

Localization of mercury in CNS of the rat. II. Intraperitoneal injection of methylmercuric chloride (CH3HgCl) and mercuric chloride (HgCl2).

The autometallographic method has been used to determine the precise localization of mercury in the brain and spinal cord of adult Wistar rats which had been treated with repeated ip injections of methylmercuric chloride (CH3HgCl; 0.2 to 10.0 mg) or mercuric chloride (HgCl2; 0.2 to 10.0 mg). The distribution of mercury was uneven following administration of HgCl2, while it was fairly homogeneous following CH3HgCl. With both compounds, however, heavy deposits of mercury were present in the motor nuclei of rhombencephalon. In contrast, cerebellar Purkinje cells, Golgi cells, and Golgi epithelial cells only contained mercury in sections from rats exposed to CH3HgCl. In cerebral sections from rats exposed to CH3HgCl, staining intensity in cortical cells varied among the layers, being greatest in laminae III, V, and VI. On the other hand, sections from rats exposed to HgCl2 showed only staining in scattered cells of lamina VI. Following administration of either compound, mercury was detected in the gray matter of the spinal cord mercury. Particularly large deposits were present in the anterior horn motoneurons. At the cellular level, the heaviest staining intensity was seen in neurons, although the cytoplasm of glia and ependymal cells also showed significant deposits in sections from rats exposed to CH3HgCl. In HgCl2-treated rats, the largest accumulations of mercury were seen in the neurons. The ependymal cells were stained to a lesser extent, while glia were devoid of mercury. Ultrastructurally, mercury deposits were located exclusively in lysosomes. The present results demonstrate that the pattern of mercury distribution and its staining intensity in individual cells in the rat CNS are dependent upon the chemical structure of the compound and the duration of its administration.

Animals↗
PubMed1990

Histochemical demonstration of mercury in the olfactory system of salmon (Salmo salar L.) following treatments with dietary methylmercuric chloride and dissolved mercuric chloride.

The deposition of organic and inorganic mercury compounds was studied histochemically in the salmon (Salmo salar L.) olfactory system. One group of salmon was given fodder pellets containing methylmercuric chloride (CH3HgCl, 99 micrograms Hg/g) for 4 weeks. Other groups of fish were exposed to dissolved mercuric chloride (HgCl2, 270 micrograms Hg/liter) for 2, 6, and 12 hr, respectively. In both series of experiments, the radioisotope 203Hg was included in order to determine the accumulation of mercury in the olfactory system. Gamma-spectrometry showed that both mercury compounds accumulated in the olfactory rosettes and their nerves. Tissue sections from the rosettes and olfactory nerves were subjected to autometallographic silver enhancement, thereby rendering mercury deposits visible for light and electron microscopy. Microscopic analysis demonstrated an intense and comprehensive Hg deposition in the axons and Schwann cells of both methylmercury- and inorganic mercury-exposed fish. On the other hand, the two mercury compounds showed different staining patterns in the sensory epithelium. The silver grains evoked by methylmercury were localized predominantly in lysosome-like inclusions within the receptor cells, while those produced by HgCl2 exposure were situated mainly along the borders of neighboring cells. The present findings that organic and inorganic mercury compounds were deposited in the olfactory system along its whole length, from the receptor cell apices to the brain, support the electrophysiological results presented elsewhere (Baatrup et al., 1990, Ecotoxicol. Environ. Safety 20, 269-276).

Administration, Oral↗
PubMed1991

Ultrastructural demonstration of mercury in Sertoli and Leydig cells of the rat following methyl mercuric chloride or mercuric chloride treatment.

The autometallographic silver enhancement technique has been used to demonstrate the ultrastructural localization of mercury in the testes of adult rats. Administration of mercuric chloride or methyl mercuric chloride in the drinking water (20 mg/L for 12 weeks) resulted in intracellular accumulations of mercury in the interstitial Leydig cells as well as in the Sertoli cells of the seminiferous tubules.

Animals↗
PubMed2003

Comparing polyaluminum chloride and ferric chloride for antimony removal.

Antimony has been one of the contaminants required to be regulated, however, only limited information has been collected to date regarding antimony removal by polyaluminium chloride (PACl) and ferric chloride (FC). Accordingly, the possible use of coagulation by PACl or FC for antimony removal was investigated. Jar tests were used to determine the effects of solution pH, coagulant dosage, and pre-chlorination on the removal of various antimony species. Although high-efficiency antimony removal by aluminum coagulation has been expected because antimony is similar to arsenic in that both antimony and arsenic are a kind of metalloid in group V of the periodic chart, this study indicated: (1) removal density (arsenic or antimony removed per mg coagulant) for antimony by PACl was about one forty-fifth as low as observed for As(V); (2) although the removal of both Sb(III) and Sb(V) by coagulation with FC was much higher than that of PACl, a high coagulant dose of 10.5mg of FeL(-1) at optimal pH of 5.0 was still not sufficient to meet the standard antimony level of 2 microg as SbL(-1) for drinking water when around 6 microg as SbL(-1) were initially present. Consequently, investigation of a more appropriate treatment process is necessary to develop economical Sb reduction; (3) although previous studies concluded that As(V) is more effectively removed than As(III), this study showed that the removal of Sb(III) by coagulation with FC was much more pronounced than that of Sb(V); (4) oxidation of Sb(III) with chlorine decreased the ability of FC to remove antimony. Accordingly, natural water containing Sb(III) under anoxic condition should be coagulated without pre-oxidation.

Aluminum Hydroxide↗
PubMed1997

Topiramate enhances GABA-mediated chloride flux and GABA-evoked chloride currents in murine brain neurons and increases seizure threshold.

The anticonvulsant topiramate is effective in laboratory animals against maximal electroshock seizures, amygdala kindling, and spike-wave discharges and has demonstrated efficacy in humans for the treatment of complex partial seizures. However, its mechanism of action has yet to be clearly elucidated. When the chloride-sensitive fluorescent probe N-(ethoxycarbonylmethyl)-6-methoxyquinolinium bromide (MQAE) was used as a tool for estimating the effect of anticonvulsant drugs on GABA receptor function, topiramate was observed to enhance GABA-stimulated chloride (Cl-) flux. At a therapeutic concentration, topiramate (10 microM) enhanced GABA-stimulated (10 microM) Cl- influx into cerebellar granule neurons but did not significantly increase Cl- influx alone. Phenytoin (10 microM) and acetazolamide (300 microM) did not enhance GABA-stimulated Cl- influx. In patch-clamp electrophysiological studies, topiramate also enhanced GABA-evoked whole cell Cl- currents in mouse cerebral cortical neurons in culture. In vivo anticonvulsant studies confirmed that topiramate, like phenytoin, is primarily effective against tonic extension seizures induced by maximal electroshock and is ineffective against clonic seizures induced by the subcutaneously administered chemoconvulsants pentylenetetrazol (PTZ), bicuculline (Bic), and picrotoxin (Pic). In contrast to phenytoin, topiramate, at a dose equivalent to the MES median effective dose (ED50), was found to elevate seizure threshold as estimated by the intravenous PTZ seizure threshold test. Taken together these results support the conclusion that enhancement of GABA-mediated Cl- flux may represent one mechanism that contributes to the anticonvulsant activity of topiramate.

Animals↗
PubMed1975

Chloride flux in bilayer membranes: chloride permeability in aqueous dispersions of single-walled, bilayer vesicles.

Aqueous dispersions of phosphatidylcholine vesicles were utilized to determine bilayer permeability to 36-Cl as a function of pH and temperature. These dispersions were comprised of single-walled vesicles, homogeneous in size, prepared by sonication of purified egg phosphatidylcholine under argon followed by fractionation on a molecular sieve. Permeability constants calculated from the inward flux of 36-Cl and the geometric parameters of these vesicles proved to be dependent on both pH and temperature. Analysis of these dependences leads to the conclusion that 36-Cl permeation in the presence of KCl is due principally to a carrier mediated exchange process involving a phospholipid-HCL complex. Net permeation by H-36-Cl may make a small contribution to the 36-Cl flux, however, studies carried out at very low chloride concentrations show that this flux is much smaller than the exchange flux. Thus chloride permeability for the exchange process is 1.5 times 10- minus 11 cmsec- minus 1 while the corresponding coefficient for the net flux of H-36-Cl is 1.0 times 10- minus 12 cm sec- minus 1 at pH 7. The activation energy for the 36-Cl exchange flux was found to be 19 plus or minus 2 kcal/mol. This value is similar to that obtained for the transbilayer "flip-flop" of phosphatidylcholine molecules in a similar system (Kornberg and McConnell, 1971). This correspondence together with the fact that the experimentally determined flux of 36-Cl agrees well with that calculated from the "flip-flop" parameters, strongly suggests that the flux of 36-Cl and "flip-flop" of phosphatidylcholine may be the same process.

Binding Sites↗
PubMed2004

Tolerance for excess basic zinc chloride and basic copper chloride in chicks.

(1) Four chick experiments were conducted to determine toxicity estimates for basic zinc chloride (BZC) and basic copper chloride (BCC), now being used as sources for these minerals. (2) In experiment 1, New Hampshire x Columbian crossbred chicks were fed 0, 500, 1000, 1500, 3000 and 5000 mg Zn/kg from BZC (Zn5Cl2(OH)8). Broken-line regression analysis showed that the minimal toxic break points for chick weight gain and gain:food were 1720 and 2115 mg Zn/kg, respectively. (3) Crossbred chicks were fed 0, 150, 250, 500, 750 and 1000 mg Cu/kg from BCC (Cu2(OH)3C) in experiment 2. Regression analysis indicated that the minimal toxic break points for chick weight gain and gain:food were 642 and 781 mg Cu/kg, respectively. (4) In experiment 3, commercial broiler chicks were fed 0, 1500, 2000 and 2500 mg supplemental Zn/kg from BZC or 0, 500, 650 and 800 mg supplemental Cu/kg from BCC. Broiler chicks fed those high inclusion rates of Zn did not show reduced weight gain in comparison to chicks fed no supplemental Zn. All high concentrations of supplemental Cu depressed chick weight gain in comparison to control chicks. (5) Experiment 4 involved two separate 4 x 2 factorial designs with supplemental Zn (0, 2500, 3500 and 4500 mg/kg) or Cu (0, 500, 750 and 1000 mg/kg) and two breeds of chicks (crossbred and commercial). Significant interactions for weight gain, food intake, gain:food and liver Cu suggested that the crossbred and commercial chicks responded differently to high concentrations of supplementary dietary Cu.

Animals↗
PubMed1977

A dominant lethal study in male rats after repeated exposures to vinyl chloride or vinylidene chloride.

Male CD rats were exposed 6 hr/day for 5 days/wk to 0, 50, 250, or 1,000 ppm of vinyl chloride or 55 ppm of vinylidene chloride. Starting on week 11 of exposure, these males were mated with untreated females. There was no evidence of either preimplantation loss or postimplanation loss in pregnant females that resulted from these matings. Consequently, it was concluded that these exposures did not produce germinal mutation, as manifested by a dominant lethal effect, in male rats.

Animals↗
PubMed1978

Carcinogenicity of vinyl chloride and vinylidene chloride.

Exposure of mice to 50, 250, or 1000 ppmm of vinyl chloride (VC) in the air for 6 h/d, 5 d/wk, caused a high incidence of bronchioloalveolar adenoma, mammary gland tumors, and hemangiosarcoma. Mammary gland tumors occurred in the females and included ductular adenocarcinoma and squamous and anaplastic cell carcinomas with metastasis to the lung. Hemangiosarcoma occurred in the liver and, to a lesser extent, in various other organs. The incidence and severity of these tumors increased with the concentration of VC and the length of exposure. Malignant lymphoma involving various organs was observed in several mice. Rats were more resistant to the carcinogenic effects of VC. Exposure of rats to 250 or 1000 ppm of VC caused hemangiosarcoma in the liver. Many rats with hepatic hemangiosarcoma also developed hemangiosarcoma in the lung. Extrahepatic hemangiosarcoma also occasionally occurred in other organs. Exposure to 55 ppm of vinylidene chloride (VDC) caused hepatic hemangiosarcoma and probably bronchioloalveolar adenoma in mice. Hemangiosarcoma also occurred in the mesenteric lymph node or subcutaneous tissue in two rats exposed to 55 ppm of VDC.

Aerosols↗
PubMed1981

Follow-up study on the carcinogenicity of vinyl chloride and vinylidene chloride in rats and mice: tumor incidence and mortality subsequent to exposure.

Carcinogenic and other toxic effects in rats and mice were examined during a 12-mo period following exposure to vinyl chloride (VC) or vinylidene chloride (VDC). Exposure of male and female mice to 50, 250, or 1000 ppm VC for 6 h/d, 5 d/wk, for 1, 3, or 6 mo resulted in increased numbers of deaths and increased moribundity at all dose levels during the exposure and postexposure periods, as compared with air-exposed controls. Similar observations were made with rats after 1, 3, 6, or 10 mo exposure to VC. Cumulative tumor incidence at various organ sites also increased in both species during the postexposure period in proportion to dose or duration of exposure at higher dose levels. However, except for mammary gland tumors in female mice, no significant increase in cumulative tumor incidence occurred in either species at 50 ppm VC or 55 ppm VDC, regardless of duration of exposure. These results suggest that exposure to vinyl halides at dose levels lower than those that elicit a significant increase in cancer incidence during the lifetime of the animal may, nonetheless, increase the risk of early death or moribundity from toxic pre- or subcarcinogenic effects. At dose levels higher than those consistent with the physiological defense or repair capabilities of the cell, ultimate tumor incidence becomes proportionate to length of exposure and may reflect the number of carcinogenic events elicited during the exposure period.

Animals↗
PubMed1992

Toxicokinetics of mercuric chloride and methylmercuric chloride in mice.

Future human exposure to inorganic mercury will probably lead to a few individuals occupationally exposed to high levels and much larger populations exposed to low or very low levels from dental fillings or from food items containing inorganic mercury; human exposure to methylmercury will be relatively low and depending on intake of marine food. Ideally, risk assessment is based on detailed knowledge of relations between external and internal dose, organ levels, and their relation to toxic symptoms. However, human data on these toxicokinetic parameters originate mainly from individuals or smaller populations accidentally exposed for shorter periods to relatively high mercury levels, but with unknown total body burden. Thus, assessment of risk associated with exposure to low levels of mercury will largely depend on data from animal experiments. Previous investigations of the toxicokinetics of mercuric compounds almost exclusively employed parenteral administration of relatively high doses of soluble mercuric salts. However, human exposure is primarily pulmonary or oral and at low doses. The present study validates an experimental model for investigating the toxicokinetics of orally administered mercuric chloride and methylmercuric chloride in mice. Major findings using this model are discussed in relation to previous knowledge. The toxicokinetics of inorganic mercury in mice depend on dose size, administration route, and sex, whereas the mouse strain used is less important. The "true absorption" of a single oral dose of HgCl2 was calculated to be about 20% at two different dose levels. Earlier studies that did not take into account the possible excretion of absorbed mercury and intestinal reabsorption during the experimental period report 7-10% intestinal uptake. The higher excretion rates observed after oral than after intraperitoneal administration of HgCl2 are most likely due to differences in disposition of systemically delivered and retained mercury. After methylmercury administration, mercury excretion followed first-order kinetics for 2 wk, independently of administration route, strain, or sex. However, during longer experimental periods, the increasing relative carcass retention (slower rate of excretion) caused the elimination to deviate from first-order kinetics. Extensive differences in the toxicokinetics of methylmercury with respect to excretion rates, organ deposition, and blood levels were observed between males and females.(ABSTRACT TRUNCATED AT 400 WORDS)

Absorption↗
PubMed1979

Comparison of the chloride electrode and gravimetric chloride titration sweat tests.

The chloride electrode sweat test and gravimetric chloride titration technic are compared. The two technics gave comparable mean values, ogives, equivalent points, and overlap for patients with cystic fibrosis and healthy subjects. As a single test with either technic has an unacceptable risk for false-positive or false-negative results, tests should always be done in pairs. A statistical interpretation technic based on prevalence and technical variability of the two tests will decrease the number of undiagnosed subjects and will define probability of cystic fibrosis in the undiagnosed group.

Chlorides↗
PubMed2003

Protective effects of dietary potassium chloride on hemodynamics of Dahl salt-sensitive rats in response to chronic administration of sodium chloride.

BACKGROUND: Dietary potassium supplementation decreases blood pressure and prevents strokes in humans, and prevents strokes and renal damage in Dahl salt-sensitive (DSS) rats. OBJECTIVE: To study the effects of various concentrations of dietary potassium chloride (KCl) on the hemodynamics of Dahl salt-resistant (DSR) and DSS rats receiving a 1% sodium chloride (NaCl) diet for 8 months, to determine whether there is an optimal dietary concentration of KCl that minimizes increases in blood pressure and causes least impairment of blood flow in the brain and kidneys. METHODS AND RESULTS: We found a biphasic effect on hemodynamic parameters as a function of dietary KCl in DSS rats of the Rapp strain fed 1% NaCl with increasing dietary KCl (0.7, 2.6, 4 and 8%). After 8 months receiving a diet containing 1% NaCl and 0.7% KCl, DSS rats had mean arterial pressures (MAP), plasma volumes, cardiac outputs and renal and cerebral vascular resistances that were significantly increased compared with those of DSR rats receiving the same diet. With a 2.6% KCl diet, all these parameters were significantly reduced compared with those in DSS rats fed the 0.7% KCl diet and were similar to those in DSR rats fed 2.6% KCl. Total peripheral resistance in DSR and DSS rats was similar on all diets. When KCl was increased to 4 and 8%, MAP, plasma volume, cardiac output and renal vascular resistance progressively increased in DSR and DSS rats, without changing total peripheral resistance. These changes paralleled increases in plasma aldosterone, which resulted from adrenocortical stimulation by the increasing dietary KCl; however, cerebral vascular resistance of DSR and DSS rats decreased significantly with a 4% KCl diet, despite increased aldosterone and sodium retention. Only DSS rats fed a 2.6% KCl diet had hemodynamics similar to those of DSR control rats fed the same diet, and hyperaldosteronism, sodium retention and increased plasma volume did not occur. CONCLUSION: 'Optimal' dietary KCl (2.6%) prevents hypertension and preserves cerebral and renal hemodynamics in DSS rats fed a diet containing 1% NaCl for 8 months, which causes hypertension when dietary KCl is limited or excessive.

Aldosterone↗
PubMed2004

Investigations of pharmacologic properties of the renal CLC-K1 chloride channel co-expressed with barttin by the use of 2-(p-Chlorophenoxy)propionic acid derivatives and other structurally unrelated chloride channels blockers.

CLC-K chloride channels are expressed in the kidney, where they play a pivotal role in the mechanisms of urine concentration and Na(+) reabsorption. The identification of barttin as an essential beta-subunit of CLC-K channels allowed performance of a pharmacologic characterization of wild-type CLC-K1 expressed in Xenopus oocytes. To this end, a series of 2-(p-chlorophenoxy)propionic acid (CPP) derivatives were screened using the two-microelectrode voltage-clamp technique. Several chemical modifications regarding the phenoxy group of the side chain (elimination of the oxygen atom or of methylenic groups, substitutions of the chlorine atom) did not alter the drug blocking activity, with five different derivatives showing a similar potency. Among these, a derivative of CPP carrying a benzyl group on the chiral center in the place of the methyl group represented the minimal structure for blocking CLC-K1. It inhibited the channel from the extracellular side with an affinity in the 150 micro M range. The blocking potency of this compound is fourfold increased by lowering the extracellular chloride concentration, suggesting that the drug interacts with the channel pore. Concomitantly, the effect of some "classical" Cl(-) channel blockers (9-anthracenecarboxylic acid, 2-(phenylamino)benzoic acid, iminodibenzoic acid, niflumic acid, 5-nitro-2-(3-phenylpropylamino)benzoic acid, 4,4'-diisothiocyanato-2,2'-stilbenedisulfonic acid disodium salt, and 4-acetamido-4'-isothiocyanato-2,2'-stilbenedisulfonic acid disodium salt) was screened. 4,4'-Diisothiocyanato-2,2'-stilbenedisulfonic acid disodium salt was the only one capable of blocking CLC-K1 with a potency similar to the CPP derivative, although in an irreversible manner. The newly identified substances provide a useful tool to investigate the biophysical and physiologic role of these renal channels and a starting point for the development of therapeutic drugs with diuretic action.

2-Methyl-4-chlorophenoxyacetic Acid↗