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PubMed1995

Cyclic AMP-related and cation-affected human platelet chloride transport regulation.

Cystic fibrosis has been characterized as a defect in the regulation of cyclic AMP-dependent transepithelial chloride transport. The activation of cyclic AMP-dependent protein kinase A by cyclic AMP occurs normally in cystic fibrosis cells, but they fail to transport chloride ions in response to protein kinase A stimulation. Defective chloride secretion and abnormal electrolyte transport occurs in several organs including the lung, sweat glands, intestine and pancreas. The present work was aimed at exploring whether the same or similar regulatory systems are functional in platelets, and if they are altered or deficient in individuals with cystic fibrosis. Chloride transport in platelets from normal subjects and from cystic fibrosis patients was measured by cell sizing techniques where chloride permeability is the limiting factor. In platelets from healthy volunteers, the chloride channel blocker, 5-nitro-2-(3-phenylpropylamino) benzoic acid, inhibits the transport in a dose-dependent manner. The preservation of chloride transport capability is shown to be dependent upon the presence of either Ca2+ or two divalent cation substitutes, Cd2+ or Cu2+. It is also shown that in normal subjects 0.1 mumol/l prostaglandin E1, which elevates cyclic AMP 6 times and abolishes platelet aggregation, significantly enhances the rate constant of the transport. Furthermore, in five out of nine cystic fibrosis patients studied, platelet chloride transport did not respond to stimulation by prostaglandin E1.

Adolescent↗
PubMed2006

Control of mammalian cochlear amplification by chloride anions.

Chloride ions have been hypothesized to interact with the membrane outer hair cell (OHC) motor protein, prestin on its intracellular domain to confer voltage sensitivity (Oliver et al., 2001). Thus, we hypothesized previously that transmembrane chloride movements via the lateral membrane conductance of the cell, GmetL, could serve to underlie cochlear amplification in the mammal. Here, we report on experimental manipulations of chloride-dependent OHC motor activity in vitro and in vivo. In vitro, we focused on the signature electrical characteristic of the motor, the nonlinear capacitance of the cell. Using the well known ototoxicant, salicylate, which competes with the putative anion binding or interaction site of prestin to assess level-dependent interactions of chloride with prestin, we determined that the resting level of chloride in OHCs is near or below 10 mm, whereas perilymphatic levels are known to be approximately 140 mm. With this observation, we sought to determine the effects of perilymphatic chloride level manipulations of basilar membrane amplification in the living guinea pig. By either direct basolateral perfusion of the OHC with altered chloride content perilymphatic solutions or by the use of tributyltin, a chloride ionophore, we found alterations in OHC electromechanical activity and cochlear amplification, which are fully reversible. Because these anionic manipulations do not impact on the cation selective stereociliary process or the endolymphatic potential, our data lend additional support to the argument that prestin activity dominates the process of mammalian cochlear amplification.

Animals↗
PubMed1983

Sodium chloride for broiler breeders.

Two experiments, each of 224 days duration, were conducted with Cobb broiler breeders, 32 weeks of age, to determine their response to supplemental dietary sodium chloride levels ranging from .12 to .48% in a corn-soybean meal diet. Average hen-day egg production, daily feed intake, feed required per dozen eggs, and egg specific gravity were not significantly influenced by any level of supplemental sodium chloride. Egg weights from hens receiving .36% sodium chloride were significantly heavier than those of birds that consumed .12 and .24% sodium chloride but not those of the .18 and .48% sodium chloride treatments. Egg fertility was significantly depressed by .48% sodium chloride and numerically reduced by .36%. Hatchability of fertile eggs was not found to be affected, but overall hatchability of eggs from .36 and .48% supplemental sodium chloride treatments was significantly lower than that supported by the least sodium chloride level provided, .12%. These data indicate that current National Research Council (1977) sodium requirements for heavy breeders (200 mg/day) may provide at least 23% more sodium than is required (less than or equal to 154 mg/day) and that daily sodium intakes in the range of 320 to 420 mg may reduce fertility in broiler breeders.

Animals↗
PubMed1998

Is low serum chloride level a risk factor for cardiovascular mortality?

BACKGROUND: Serum chloride level is routinely assayed in clinical laboratories in the management of patients with kidney disorders and with metabolic diseases. It is a biological parameter that is easily, precisely and relatively cheaply measured. The epidemiological features of serum chloride levels have not been studied before. METHODS: For the random sample of men and women from the Belgian Interuniversity Research on Nutrition and Health aged 25-74 years, free of symptomatic coronary heart disease at baseline, serum chloride concentrations were measured, among those of other electrolytes. The cohort was followed up for 10 years with respect to subsequent cause-specific mortality. RESULTS: The results are based on observations of 4793 men and 4313 women. According to Cox regression analysis serum chloride level was one of the strongest predictors of total, cardiovascular disease (CVD) and non-CVD mortalities independently of age, body mass index, sex, smoking, systolic blood pressure, levels of total and high-density lipoprotein cholesterol, uric acid, serum creatinine and serum total proteins and intake of diuretics. This relation was proved to be independent of levels of other serum electrolytes and similar for men and women. The estimated adjusted risk ratio for CVD death for subjects with a serum chloride level < or =100 mmol/l compared with those with levels above that limit was 1.65 (95% confidence interval 1.06-2.57) for men and 2.16 (95% confidence interval 1.11-4.22) for women. The study of adjusted risk ratios for four groups of subjects defined on the basis of their baseline serum chloride levels revealed a decreasing log-linear 'dose-response' relation to total and cardiovascular mortalities. CONCLUSION: This s the first report from a population-based study to indicate that there is an association between serum chloride level and the incidence of total, CVD and non-CVD mortalities. The risk ratio for CVD mortality associated with a low serum chloride level was comparable to or higher than those observed for well-established CVD risk factors.

Adult↗
PubMed1996

Effect of sodium chloride- and sodium bicarbonate-rich mineral water on blood pressure and metabolic parameters in elderly normotensive individuals: a randomized double-blind crossover trial.

OBJECTIVE: To examine the effect of sodium chloride- and sodium bicarbonate-rich mineral water on blood pressure and parameters of glucose and lipid metabolism in elderly normotensive individuals. METHODS: We examined 21 healthy men and women aged 60-72 years in a randomized, placebo-controlled, double-blind crossover trial. After reducing dietary salt intake to below 100 mmol/day, study participants were randomly assigned to drink 1.5 l daily of a sodium chloride-rich (sodium 84.5 mmol/l, chloride 63.7 mmol/l, bicarbonate 21.9 mmol/l), a sodium bicarbonate-rich (sodium 39.3 mmol/l, chloride 6.5 mmol/l, bicarbonate 48.8 mmol/l) and a low-sodium (placebo: sodium, chloride and bicarbonate < 0.02 mmol/l) mineral water for 4 weeks each in a three-phase crossover order. Each phase was separated by a 2-week washout period in which the study participants remained on a low-salt diet. Compliance was assessed by biweekly urinary electrolyte excretion and five study participants were excluded from analysis for failing to complete the trial or to fulfil the compliance criteria. RESULTS: Mean arterial blood pressure was significantly lower during the periods of consuming low-sodium -7.0 +/- 7.2 mmHg, P < 0.001) or sodium bicarbonate-rich (-5.7 +/- 6.4 mmHg, P < 0.05) water than at baseline. In contrast, blood pressure during the phase of drinking sodium chloride-rich water was identical to that at baseline. Ambulatory 24 h blood pressure, oral glucose tolerance and plasma lipids were not affected by the different regimens. Urinary calcium excretion was significantly reduced by drinking low-sodium or sodium bicarbonate-rich water but was unchanged under the sodium chloride-rich water. CONCLUSION: Consumption of sodium chloride-rich mineral water can abolish the blood pressure reduction induced by dietary salt restriction in elderly individuals. Sodium bicarbonate-rich mineral water in conjunction with a low-salt diet may have a beneficial effect on calcium homeostasis.

Aged↗
PubMedDate not supplied

[The extracellular ionic environment and bone metabolism. In vitro study of the role of chloride].

Controversies surround the view that the blood-bone ionic equilibrium is controlled by ionic changes at a so called "bone membrane" that display a pump-leak mechanism able to maintain a concentration gradient for chloride in addition to that for calcium, sodium and potassium. On the other hand it is known that a chloride-bicarbonate transport is active at bone cells membrane to control cytosolic pH. We tested the hypothesis that a modification of the chloride concentration of the culture medium, as well as a block of the chloride-bicarbonate transport by an anionic channels blocker, in an experimental model that keeps intact the bone membrane, may influence the bone cells activity and that the influence may be quantitatively different to that previously observed in isolated bone cells. The experimental model is the intact fetal rat limb bone, cultured for 24 hours in a simplified medium at different chloride concentrations obtained by substituting chloride with isethionate. Alkaline phosphatase activity released in the medium was measured as a marker of osteoblasts activity. By progressively reducing the chloride concentration from 117 mM to 29 mM, alkaline phosphatase activity was found unchanged. By dramatically reducing the medium chloride concentration to the range 14-0 mM, alkaline phosphatase activity was significantly (p = 0.0002) inhibited by 31.58%.(ABSTRACT TRUNCATED AT 250 WORDS)

Alkaline Phosphatase↗
PubMed1975

The effect of potassium chloride on the Bohr effect of human hemoglobin.

The normal and differential titration curves of liganded and unliganded hemoglobin were measured at various KCl concentrations (0.1 to 2.0 M). In this range of KCl concentrations, the curves for deoxyhemoglobin showed no salt-induced pK changes of titratable groups. In the same salt concentration range oxyhemoglobin showed a marked change in titration behavior which could only be accounted for by a salt-induced increase in pK of some titratable groups. These results show that the suppression of the alkaline Bohr effect by high concentrations of neutral univalent salt is not caused by a weakening of the salt bridges in deoxyhemoglobin but is due to an interaction of chloride ions with oxyhemoglobin. Measurements of the Bohr effect at various KCl concentrations showed that at low chloride ion concentration (5 times 10-3 M) the alkaline Bohr effect is smaller than at a concentration of 0.1 M. This observation indicates that at a chloride ion concentration of 0.1 M, part of the alkaline Bohr effect is due to an interaction of chloride ions with hemoglobin. Furthermore, at low concentrations of chloride ions the acid Bohr effect has almost vanished. This result suggests that part of the acid Bohr effect arises from an interaction of chloride ions with oxyhemoglobin. The dependence of the Bohr effect upon the chloride ion concentration can be explained by assuming specific binding of chloride ions to both oxy- and deoxyhemoglobin, with deoxyhemoglobin having the highest affinity.

Binding Sites↗
PubMed1990

Changes in distribution of chloride ions in embryonic chicken retinal pigment epithelium.

Changes in the distribution pattern of chloride ions were studied in the embryonic chicken retinal pigment epithelium (RPE), chloride ions being deposited as silver chloride (AgCl) in the RPE and observed by electron microscope. Before the 7th day after fertilization, the chloride ions did not accumulate anywhere in the tissue. From the 8th day, the chloride ions accumulated in the cytoplasm and the intercellular space, first in the posterior fundus RPE and later in the anterior fundus RPE. Melanin pigment granules and apical microvilli of the RPE developed from the posterior fundus toward the anterior fundus in parallel with the changes in the distribution pattern of chloride ions. These results suggest that the chloride ion transport function of the RPE appears first in the posterior fundus on the 8th day after fertilization and thereafter the development of the chloride ion transport moves to the anterior fundus. This development of the transport function appears to progress in parallel with the morphological development of the RPE cells.

Animals↗
PubMed1990

Quantification of chloride in sweat with the Cystic Fibrosis Indicator System.

We examined the relation between chloride concentration and the area of complexed chloride of Medtronic's Cystic Fibrosis Indicator System, using a high-resolution x-y coordinated digitizer to measure the circumference of the chloride precipitation ring. These digitized points were entered directly into an IBM PC computer, where the area of the chloride precipitation was calculated with use of a repetitive rectangular estimation program. Using these data, we determined the relationship between the area of chloride precipitation and the chloride concentration of the standard NaCl solutions. When the area of the ring of chloride precipitation in the system's patch is measured immediately after the sweat test is completed, the concentration of chloride in the sweat can be calculated with a reproducibility equal to that of the Gibson-Cooke sweat test.

Chlorides↗
PubMed1986

Anesthetic and convulsant barbiturates alter gamma-aminobutyric acid-stimulated chloride flux across brain membranes.

gamma-Aminobutyric acid (GABA), the major inhibitory neurotransmitter in the mammalian brain, increases membrane chloride conductance. Previously, the authors reported that GABA increases 36Cl- uptake by membrane vesicles (microsacs) prepared from mouse brain. In the present study, we examined the actions of barbiturates on basal and GABA-stimulated chloride influx by brain vesicles. The anesthetic barbiturates pentobarbital, phenobarbital, mephobarbital, amobarbital, hexobarbital and R-(-)-1-methyl-5-phenyl-5-propyl barbiturate enhanced GABA-dependent chloride flux. Barbiturate enhancement of GABA action was seen at concentrations that are subanesthetic in vivo (e.g., 10 microM pentobarbital was effective). Pentobarbital was about 10 times more potent than pentobarbital, suggesting that chloride flux is related to the sedative rather than anticonvulsant actions of barbiturates. Pentobarbital (1 mM) prevented the antagonism of GABA-stimulated 36Cl- produced by picrotoxinin. The barbiturates generally produced no change in GABA-independent flux, although large concentrations of pentobarbital or hexobarbital produced a slight enhancement of chloride flux in the absence of GABA. The convulsant barbiturate S-(+)-1-methyl-5-phenyl-5-propyl barbiturate inhibited GABA-stimulated chloride flux, an action opposite to that of its anesthetic enantiomer. These experiments provide evidence for a functional coupling among GABA and barbiturate receptors and the chloride ionophore and suggest that the GABA-activated chloride channel is a site of action for intoxicant-anesthetic and convulsant barbiturates.

Animals↗
PubMed1988

Transmembrane chloride flux is required for target cell lysis but not for Golgi reorientation in cloned cytolytic effector cells. Golgi reorientation, N alpha-benzyloxycarbonyl-L-lysine thiobenzyl ester serine esterase release, and delivery of the lethal hit are separable events in target cell lysis.

Cell-mediated cytotoxicity can be inhibited by the replacement of chloride with ions that are incapable of passing through chloride channels or by the presence of stilbene disulfonate derivatives known to interfere with chloride flux. We show that the stilbene disulfonate (4,4-diisothiocyano-2,2'-disulfonic acid stilbene (DIDS) inhibits lysis of YAC-1 targets by the cloned cell line NKB61A2. Inhibition of lysis occurs on the level of the effector cell inasmuch as preincubation of effectors but not of targets interferes with subsequent lysis. Moreover, inhibition of chloride flux in the target does not interfere with target cell lysis by cytotoxic granules isolated from killer cells. Target cell binding takes place in the presence of DIDS or absence of external chloride, suggesting that events that follow target cell binding require chloride flux. We show that reorientation of the Golgi apparatus, which occurs subsequent to target cell binding in the effector cell, occurs under conditions that interfere with chloride flux. It is therefore suggested that events in the effector cell taking place subsequent to the Golgi apparatus reorientation reaction are inhibited and that delivery of the lethal hit is a stimulus-induced secretory event that requires transmembrane chloride flux. Delivery of the lethal hit is shown to be independent of the release of N alpha-benzyloxycarbonyl-L-lysine thiobenzyl ester (BLT) serine esterase, suggesting that cytolytic components and BLT serine esterase are likely packaged in different vesicles.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1988

Osmotic regulation of prolactin secretion. Possible role of chloride.

The role of osmotic pressure in the exocytosis of prolactin from rat pituitary tumor (GH) cells in culture was investigated. Reducing the osmotic strength of the medium from 300 mosm to 150 mosm by removal of NaCl did not alter basal secretion of prolactin but inhibited secretion stimulated by thyrotropin-releasing hormone (TRH) and forskolin. Both basal and stimulated secretion of prolactin were inhibited by increasing the osmotic strength of the medium with NaCl (IC50 at approximately 500 mosm). The stimulated release of hormone from GH-cells was independent of sodium and unaffected by replacement of sodium ion with tetramethylammonium or choline, or by addition of 500 nM tetrodotoxin. Secretagogue-stimulated release was, however, dependent upon chloride. Exchange of medium chloride with benzoate or isethionate significantly inhibited the stimulated release of prolactin (IC50 at approximately 60 mM exchange) regardless of the secretagogue utilized (phorbol ester, forskolin, depolarization plus BAY K8644, or TRH). Exchange of medium chloride with either isethionate or benzoate reduced cell volume by 10% compared to 60% for sucrose and mannitol, suggesting that inhibition of secretion by isethionate exchange was not a result of increased intracellular osmotic pressure. Complete exchange of medium chloride with isethionate did not alter equilibrium [3H]methyl-TRH binding, resting internal [Ca2+], or the [Ca2+]i response to depolarization and TRH as measured with intracellularly trapped Fura 2. Chloride removal did not change resting internal pH and recovery from an acid load as measured by the intracellular pH-sensitive dye 2',7'-bis(carboxyethyl)-5(6)-carboxyfluorescein. The stimulated secretion of prolactin was also inhibited by exchange of chloride with isethionate in normal pituitary cells in primary culture and the ability of normal cells to respond to the dopamine agonist bromocryptine was not affected by the exchange. These results suggest that exocytosis of prolactin from GH-cells and normal pituitary cells in culture is an osmotically driven process that is chloride-dependent. Stimulated release is more chloride-dependent than constitutive release. The inhibitory effect of isethionate substitution occurs after signal transduction and is distinct from the site of dopamine inhibition of prolactin release.

Animals↗
PubMed1988

Role of calcium in chloride-secreting epithelia.

There are a number of well-characterized chloride-secreting epithelia. The role of cyclic AMP in mediating chloride secretion in these tissues is well established. The role of calcium is less well established, although a substantial body of evidence points to a significant mediator role of calcium in the modulation of chloride secretion. In some of these tissues, a rise in cytosolic calcium activity in response to secretagogues may potentiate cyclic AMP effects on chloride conductance by the activation of serosally located potassium channels. In addition, in many instances, the effect of a rise in cytosolic calcium may itself be mediated by stimulation of cyclooxygenase products that themselves are known to be chloride secretagogues. Sustained chloride secretion may reflect a synergism between cyclic AMP, calcium, and prostaglandins although such a mechanism is apparent in only some but not all chloride-secreting epithelia. It is hoped that with the application of newer techniques to measure cytosolic calcium concentration and to monitor individual channel activities, we will better understand the exact role of calcium in modulating chloride transport.

Animals↗
PubMed1977

Effect of heat stable and heat labile Escherichia coli enterotoxins, cholera toxin and theophylline on unidirectional sodium and chloride fluxes in the proximal and distal jejunum of weanling swine.

Acute, isolated loops of proximal and distal jejunum of weanling swine were exposed to either heat stable porcine Escherichia coli enterotoxin, heat labile porcine Escherichia coli enterotoxin, cholera toxin or theophylline. Unidirectional sodium fluxes in response to heat stable in the proximal jejunum were dependent on the length of time that the intestinal mucosae was exposed to the enterotoxin. Net water, sodium and chloride and unidirectional sodium and chloride flux measurements in the proximal jejunum in response to each agent uniformly indicated that net secretion of fluid and electrolytes was the result of increased unidirectional sodium secretion or blood-to-lumen flux and decreased unidirectional chloride absorption or lumen-to-blood flux. In addition heat stable cholera toxin and theophylline but not heat labile decreased unidirectional chloride secretion a small but significant amount in the proximal jejunum. Sodium and chloride flux measurements in the distal jejunum demonstrated that all four secretory agents could stimulate net secretion of water, sodium and chloride in that region. The response to these secretory agents as measured by sodium and chloride unidirectional flux rates was not similar to changes observed in the proximal jejunum. In the distal small intestine, whereas heat labile cholera toxin and theophylline induced similar qualitative changes in unidirectional sodium and chloride fluxes, that induced by heat stable differed.

Animals↗
PubMed1984

Urinary chloride concentration in acute renal failure.

The present prospective study was undertaken to evaluate the usefulness of urinary chloride concentration in determining the cause of an abrupt decline in renal function. 99 patients from diverse clinical settings with multiple causes of acute renal failure were evaluated. Urinary chloride concentrations of less than 20 mEq/l were observed in most cases of reversible prerenal azotemia (20 of 21 cases) and were observed in more frequently than urinary sodium concentration of less than 20 mEq/l (13 of 21 cases, p less than 0.01). Only prerenal azotemia accompanying diuretic use was associated with high urinary chloride concentrations (57 +/- 7 mEq/l). When prerenal azotemia occurred in the setting of metabolic alkalosis with bicarbonaturia, urinary chloride was low (4.0 +/- 1.0 mEq/l) while urinary sodium was high (65.0 +/- 19.0 mEq/l). In patients with oliguric and nonoliguric acute tubular necrosis, and in patients with acute exacerbations of chronic renal failure, mean urinary chloride concentration ranged from 40 to 67 mEq/l and mean fractional excretions of chloride ranged from 7.2 to 8.4%. Only 11% of patients with oliguric and nonoliguric acute tubular necrosis had urinary chloride concentrations of less than 20 mEq/l. Urinary chloride concentrations exhibited greater sensitivity and equivalent specificity as urinary sodium concentrations in differentiating patients with reversible prerenal azotemia from those with oliguric and nonoliguric acute tubular necrosis.

Acidosis↗
PubMed1996

Effect of calcium chloride gel treatment in dairy cows on incidence of periparturient diseases.

OBJECTIVE: To determine effect of prophylactic treatment of dairy cattle with a calcium chloride gel on serum calcium concentration in the immediate postpartum period and incidence of parturient paresis, retained fetal membranes, and displacement of the abomasum. DESIGN: Randomized controlled trial. ANIMALS: 204 Holstein cows. PROCEDURE: Cows were paired according to parity, whether they had previously had parturient paresis, and expected calving date. Cows in the treatment group received doses of calcium chloride gel 12 hours before expected calving, at calving, and 12 and 24 hours after calving. Cows in the control group did not receive calcium chloride gel. RESULTS: Compared with concentration in the control cows, mean serum calcium concentration in cows treated with calcium chloride gel was significantly increased on postcalving days 1 and 2. The increase was significant only in cows that were third parity or greater. Calcium chloride gel treatment also resulted in significantly reduced incidence of parturient paresis, parturient hypocalcemia, and displaced abomasum. The incidence of parturient paresis was lower in cows that received the precalving dose of calcium chloride gel (0/39) than in cows that did not receive the precalving dose (5/63). CLINICAL IMPLICATIONS: Results suggest that periparturient prophylactic treatment of dairy cattle with an oral calcium chloride gel may be beneficial and that treatment would be most effective for cows of third parity or greater. Administration of a precalving dose of calcium chloride gel is necessary to reduce the incidence of parturient paresis, but postcalving treatment alone has other beneficial effects.

Abomasum↗
PubMed1998

Preparation of 99Tcm-MAG3: no confirmation that sodium chloride injections from plastic containers affect radiochemical purity.

Reports have suggested that when sodium chloride injections from a plastic ampoule are used during the preparation of 99Tcm-mercaptoacetyltriglycine (99Tcm-MAG3), the radiochemical purity of the final product might be reduced. A study was therefore undertaken to examine the effect of sodium chloride injections from five manufacturers on the radiochemical purity and stability of 99Tcm-MAG3. One sodium chloride injection was supplied in a glass vial, three in plastic ampoules and one in a plastic infusion bag. Three batches of sodium chloride injections from each manufacturer were tested. The radiopharmaceutical was prepared at a radioactive concentration of 1.1 GBq in 10 ml according to the instructions of the manufacturer of TechneScan MAG3. Analysis of radiochemical purity was performed by high-performance liquid chromatography immediately after preparation and 6 h later. Using 95% as the minimum acceptable radiochemical purity, all the products were satisfactory over the 6 h test period. No manufacturer's sodium chloride injection was found to have a statistically significant effect on the radiochemical purity. Based on the 15 batches of sodium chloride injection tested, this study cannot confirm that sodium chloride injections from a plastic container affect the radiochemical purity of 99Tcm-MAG3. However, in view of the known sensitivity of some 99Tcm radiopharmaceuticals to external influences, it is probably good practice to test radiochemical purity when new batches of ancillary materials, such as sodium chloride injections, are introduced.

Chromatography, High Pressure Liquid↗
PubMed1999

Chloride channel blockers attenuate the inhibition of renin secretion by angiotensin II.

The aim of this study was to assess the relevance of chloride channels to the inhibitory effect of angiotensin II (ANGII) on renin secretion. We thus examined the effects of the chloride channels blockers IAA-94 and niflumic acid, the Na-K-Cl cotransport blocker bumetanide and substitution of isethionate for extracellular chloride on the action of ANGII on renin secretion from isolated perfused rat kidneys. Renin secretion prestimulated by isoproterenol (10 nmol/l) was almost completely blocked by ANGII with a concentration yielding a half-maximal response (EC50) of around 150 nmol/l. In the presence of IAA-94 and niflumic acid the EC50 for ANGII was shifted to about 400 nmol/l. In the presence of bumetanide and isethionate renin secretion responded more sensitively to ANGII and the EC50 for ANGII was below 100 nmol/l. On the assumption that the chloride equilibrium potential in renin-secreting cells is more positive than the membrane potential, our findings would suggest that the inhibitory effect of ANGII is enhanced when chloride entry is blocked and attenuated when chloride efflux is impaired. Activation of chloride channels therefore probably contributes to the inhibitory action of ANGII on renin secretion.

Angiotensin II↗