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At least 685 records · Page 38Linked to original sources
PubMed1983

Modulation of brain S2 serotonin receptors by lithium, sodium and potassium chloride.

The effect of LiCl, NaCl, and KCl on serotonin competition for 3H-ketanserin binding to S2 serotonin receptors in homogenates of rat prefrontal cortex were investigated. LiCl was the most potent of the ionic modulators in lowering the apparent affinity of serotonin for the S2 serotonin receptor. A threshold effect was noted at 12 mM LiCl (a 60% change in IC50); at 120 mM LiCl a nine-fold shift in the serotonin IC50 was noted. 120 mM NaCl or KCl demonstrated similar effects as 12 mM LiCl in reducing serotonin's apparent affinity. These results indicated that monovalent cations modulate S2 serotonin receptor affinity for serotonin and that lithium ion is more potent than sodium or potassium.

Animals↗
PubMed1989

[Stenosing and perforated ulcers of the small intestine related to potassium chloride in enteric-coated tablets. Apropos of 11 cases].

The enteric coated KCl tablet formulation generates complications that affect selectively the small intestine. A novel 1 g KCl tablet preparation proved to be accountable for the development of a specific type of intestinal disease. 11 cases of stenotic ulcers of the proximal ileum have been treated at the Clinique chirurgicale "C" (CHRU, Nancy) since January 1986, 9 of them presenting with perforations. These 11 patients required potassium replacement, which was being supplied by the same tablet formula. A study of these 11 cases focusing on the patients history and clinical characteristics was carried out, that included both macroscopic and microscopic examinations of the lesions. Arterial and venous networks were visualized by X-ray in two surgical tissue specimens, respectively, following injection of contrast material. The authors were thus able to bring forth evidence of the clinical uniqueness (prodromal pain reminiscent of König's syndrome and peritonitis characterized by asthenia); to identify the main risk factor (i.e., reduced bowel movement); as well as describe the basic lesion (pylorus-like stenosis), and propound a novel theory concerning the etiology and the pathology of this condition. The observation of the aforementioned cases initiated a nation-wide, post-marketing pharmacological survey, which resulted, as did a similar investigation which had been carried out in the States, in the discontinuation of any treatment by this type of galenic form of the product.

Adult↗
PubMedDate not supplied

The effects of five potassium chloride preparations on the upper gastrointestinal mucosa in healthy subjects receiving glycopyrrolate.

The effects on the upper gastrointestinal tract of five different preparations of KCl were compared in 90 healthy subjects treated with glycopyrrolate. The KCl preparations studied were wax-matrix KCl, microencapsulated KCl, liquid KCl, experimental extended-release capsules, experimental extended-release tablets,and placebo. The subjects were endoscoped prior to and after seven days of dosing. Upper gastrointestinal mucosal pathology was seen with all of the potassium preparations as well as with placebo. No statistically significant differences between the various KCl groups or between KCl groups and placebo were seen. All of the lesions were superficial, except for one ulcer seen with the microencapsulated KCl. None of the subjects developed occult gastrointestinal bleeding. There were no differences in the incidence of abdominal symptoms.

Adolescent↗
PubMed2001

Expression and role of sodium, potassium, chloride cotransport (NKCC1) in mouse inner medullary collecting duct (mIMCD-K2) epithelial cells.

Loop-diuretic-sensitive 86Rb+(K+) transmembrane fluxes were determined in cells of a mouse inner medullary collecting duct cell line (mIMCD-K2). The furosemide-sensitive (0.1 mM) influx was a substantial fraction of the total influx (0.39+/-0.04 or 0.42+/-0.03, n=5 in the presence or absence of ouabain, respectively). Furosemide also reduced 86Rb+(K+) efflux by a similar fraction (0.46). RT-PCR analysis revealed expression of mRNA for the Na+-K+-2Cl- cortransporter-1 (NKCC1), but not NKCC2. Loop-diuretic-sensitive 86Rb+(K+) influx was confined to the basolateral membrane, confirming its localisation there. The physiological properties of NKCC1 expressed in mIMCD-K2 cells, including the dependence upon medium Na+, K+ and Cl- and the relative sensitivity to loop diuretics as assessed by the concentration required for half-maximal inhibition (IC50) (bumetanide 3.3+/-1.4x10-7 M>piretanide 2.5+/-0.15x10-6 M>furosemide 2.3+/-1.2x10-5 M) were typical for NKCC1. Possible functions of NKCC1 were tested; furosemide did not inhibit the majority of forskolin-stimulated secretory short-circuit current (Isc) (83.5+/-5.3% of the maintained response at 5 min). Secondly, total 86Rb+(K+) influx was stimulated markedly when external osmolarity was increased to 600 mosmol/l by mannitol due to an increase via NKCC1 from 55+/-11 to 191+/-2 nmol/106 cells per 15 min, (both n=4, P<0.01). In contrast, 10-5 M forskolin did not stimulate total 86Rb+(K+) influx. Finally, the ability of both K+ and NH4+ to compete for ouabain-insensitive 86Rb+(K+) influx via NKCC1 was confirmed with similar concentrations for half-maximal influx reduction (K0.5). Apical exposure to NH4+ elicited rapid cytosolic alkalinisation in 2',7'-bis(carboxyethyl)-5(6)-carboxyfluorescein (BCECF)-loaded epithelial layers, consistent with selective permeability of the apical membrane to NH3. Conversely, NH4+ (5 mM) at the basal cell surface resulted in progressive acidification, the initial rate being reduced by 43% by furosemide. We conclude that NKCC1 participates in selective uptake of NH4+ at the basal surface, and that IMCD may function in direct NH4+ deposition to urine.

Ammonium Chloride↗
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↗