[Arterial hypertension. Clinical experimentation with a new hypotensive comination: 10-methoxydeserpidine-benzthiazide-potassium chloride].
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Alkaloids↗
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High dietary potassium chloride intake augments rat renal mineralocorticoid receptor selectivity via 11beta-hydroxysteroid dehydrogenase.
Glucocorticoid access to renal corticosteroid receptors is regulated by 11beta-hydroxysteroid dehydrogenases (11beta-HSDs), converting 11beta-hydroxyglucocorticoids into inactive 11-ketones. This mechanism plays a key role in maintaining normal salt-water homeostasis and blood pressure. To study whether renal cortical proximal and distal tubular 11beta-HSDs are modulated, upon shifting the electrolyte status (and may thereby contribute to adjusting the salt-water homeostasis), rats were treated for 14 days with diets with low (0.058 w/w%), normal (0.58%, which is the KCl content of standard European laboratory rat food) or high (5.8%) potassium chloride content. In proximal tubules, dietary KCl had no effect regarding corticosterone 11beta-oxidation in intact cells as well as 11beta-HSD1 and 11beta-HSD2 protein (Western blotting) and mRNA levels (semi-quantitative RT-PCR). In distal tubules, the low KCl diet also had no effect. However, distal tubules of rats fed the high KCl diet showed increased corticosterone 11beta-oxidation rates (1.6-fold, P<0.01) and 11beta-HSD2 protein (4-fold, P<0.01), whereas 11beta-HSD1 protein was decreased (no longer detected, P<0.05). Distal tubular 11beta-HSD mRNA levels were not changed upon dietary treatment. Our results suggest that upon dietary KCl loading distal tubular mineralocorticoid receptor selectivity for aldosterone is increased because of enhanced corticosterone 11beta-oxidation. This may contribute to the fine-tuning of salt-water homeostasis by the kidney.
11-beta-Hydroxysteroid Dehydrogenase Type 1↗
[Reference values of sodium, potassium, chloride, calcium, inorganic phosphate and magnesium levels in the cerebrospinal fluid of children].
Concentration of sodium, potassium, chloride, calcium, inorganic phosphate and magnesium was determined in cerebrospinal fluid of 155 children (ages 1 month - 16 years). On the basis of clinical criterions the children were considered to be "healthy". The total number of examined children was 2 500 (1978-1983). The statistical age- and sexspecific investigation of the results showed no significant differences. Compilation of the values resulted in a physiological concentration of sodium 132.3 +/- 17.6 mval/l, potassium 2,59 +/- 0.37 mval/l, chloride 113.1 +/- 15.5 mval/l, calcium 3.47 +/- 1.45 mval/l, inorganic phosphate 1.11 +/- 0.21 mg/dl and magnesium 2.60 +/- 0.46 mg/dl.
Adolescent↗
Evaluation of the ulcerogenic effect of potassium chloride by endoscopy and fecal blood loss.
In a blinded-observer crossover study, 16 volunteers ingested equimolar doses of three different potassium chloride preparations and placebo for nine days in a random order. The irritating effect on the mucosa was evaluated by means of upper gastrointestinal endoscopy and fecal blood loss, measured by reference to the amount of radioactivity in three 24-hour samples after previous injection of 51Cr-tagged autologous red cells. The microencapsulated KCl capsule preparation induced three ulcers, but the total endoscopic group score was not significantly higher than the score with placebo. The total endoscopic group score for the wax-matrix formulation was significantly higher than the score for placebo (P less than .05) and for a new microencapsulated KCl tablet preparation containing a potent disintegrant (P less than .10). We did not find any significant differences in mean fecal blood loss during the four different treatments. A correlation between endoscopic score and fecal blood loss was found in the placebo group (r = .54) and the microencapsulated KCl capsule preparation (r = .56) group.
Adult↗
The treatment of Urginea sanguinea Schinz poisoning in sheep with activated charcoal and potassium chloride.
An 80% survival rate was achieved when sheep which received lethal doses of Urginea sanguinea were treated with activated charcoal at 5 g/kg and potassium chloride at 1 g/kg body mass per os. A brief description of U. sanguinea poisoning and of the mechanism of cardiac glycoside action is given. Clinical examinations, ECG recordings and serum potassium levels were done to monitor developing signs of poisoning.
Animals↗
Tumor-specific skin-reactive antigen solubilized from a syngeneic guinea pig liposarcoma by 3M potassium chloride.
Tumor-specific and skin-reactive antigen of a syngeneic liposarcoma (H-10) of Hartley/F guinea pig was solubilized with 3M potassium chloride and purified by precipitation with 2M ammonium sulfate, followed by Sephadex G-200 gel filtration. The antigenic activity of 7 fractions obtained was estimated by the delayed-type skin reaction elicited in syngeneic animals immunized with H-10 cells admixed with BCG. Accurate relative activity of the fractions comparable to the skin reaction elicited by living H-10 cells was calculated by the parallel line assay method in which the dose-response curves of the fractions are compared with that of living cells. About 30 approximately 50 microgram protein of the 3 fractions eluted slowly from the Sephadex column elicited the skin reaction equivalent to that elicited with 1 X 10(6) of living H-10 cells. Tumor-specific skin reactivity per microgram protein of these 3 fractions was roughly 20 approximately 40 times higher than that of lyophilized cells.
Animals↗
Ulceration and stricture of the esophagus due to oral potassium chloride (slow release tablet) therapy.
A patient with no pre-existing history of gastrointestinal disease developed a benign stricture of the esophagus after taking potassium chloride slow-release tablets (Slow-K) while in the recumbent position in a coronary care unit. Management by bougienage using Malloney and Eder-Puestow dilators was undertaken and although complications occurred, a reasonably satisfactory result was obtained. The literature on potassium-induced stricture of the esophagus is reviewed in order to underscore the importance and severity of this complication and to suggest that this medical problem may be entirely preventable.
Administration, Oral↗
Comparison of vasoconstrictor actions of norepinephrine and potassium chloride before and after damage of endothelium by saponin.
Using isolated and perfused mesenteric arterial preparations of dogs, vasoconstrictor responses to intraluminal norepinephrine and potassium chloride were investigated in the presence and absence of the endothelium. Intraluminal administration of saponin readily removed the endothelium. Saponin (1-3 mg) caused an increase in perfusion pressure, and then approximately 20 min later perfusion pressure became stable at a somewhat higher level than that of the control. A larger dose of saponin (10 mg) caused a tremendous but temporary increase of perfusion pressure. KCl-induced vasoconstriction was significantly enhanced by pretreatment with 0.3, 1, and 3 mg saponin, but norepinephrine-induced constriction was not modified significantly. Moreover, it was demonstrated that diltiazem, a potent Ca antagonist, inhibited the KCl-induced vasoconstriction more readily in the absence than in the presence of the endothelium.
Animals↗
In vitro evidence of tissue susceptibility rhythms. I. Temporal variation in effect of potassium chloride and phenylephrine on rat aorta.
In this study, time-dependent variations in the in vitro sensitivity of rat thoracic aorta rings to potassium chloride (KCl) and phenylephrine (Phe) were investigated. Animals were synchronized with a 12h light and 12h darkness (lights on 08:00-20:00) schedule, and thoracic aortas were obtained at six different times of the day (1, 5, 9, 13, 17, and 21 hours after lights on). In order to avoid endothelial influence, all experiments were performed in endothelium-denuded preparations. Responses to KCI showed time-dependent variations in all the concentrations used. Phe-induced contractions also exhibited time-dependent differences. The rhythmic pattern of Phe responses did not change with the presence of the alpha1-adrenergic antagonist prazosin. In addition, both the EC50 values of KCl and Phe, and also the K(B) values of prazosin, displayed rhythmicity. In conclusion, time of obtaining tissues is an important factor for experimental standardization in, at least, vascular smooth muscle preparations.
Activity Cycles↗
The treatment of Moraea polystachya (Thunb) KER-GAWL (cardiac glycoside) poisoning in sheep and cattle with activated charcoal and potassium chloride.
Six out of 6 steers survived a lethal dose of Moraea polystachya (blue tulp) when treated with activated charcoal alone and 3 out of 4 wethers survived when treated with activated charcoal plus potassium chloride. Barbeque charcoal was not of therapeutic value. An increase in the level of serum potassium served as indicator of acute poisoning in only a third of the animals.
Animals↗
The role of the vascular endothelium in the contractile responses of human chorionic plate artery in pre-eclampsia to prostaglandin F2 alpha, 5-hydroxytryptamine, and potassium chloride.
This study characterises the reactivity of chorionic plate artery in pre-eclampsia to prostaglandin F2 alpha (PGF2 alpha), 5-hydroxytryptamine (5-HT), and potassium chloride (KCl) and examines the role of the vascular endothelium in these responses. Ring segments of the chorionic plate arteries of women after normal and pre-eclamptic pregnancies were contracted by PGF2 alpha, 5-HT, and KCl. The experiments were carried out in the presence and absence of endothelium, and on intact rings treated with 10(-6)M indomethacin. The maximal contractile responses of rings from pre-eclamptic women to 5-HT, PGF2 alpha, or KCl were significantly greater than those of rings from normotensive pregnant women. The EC50 values of responses were significantly lower in rings from pre-eclamptic subjects. Endothelium removal and treatment of the rings with indomethacin had no effect on the contractile responses of rings from normotensive pregnant women to all the agents, but significantly increased the EC50 value and decreased the maximal contractile responses of rings from pre-eclamptic women to 5-HT and PGF2 alpha. While de-endothelialisation increased the EC50 value for responses of the rings from pre-eclamptic women to KCl, pretreatment with indomethacin did not significantly affect the KCl-induced responses. The results of the study suggest that pre-eclampsia enhanced the reactivity of human chorionic plate artery to 5-HT, PGF2 alpha, and KCl through the involvement of endothelial derived contracting factors. The increased responses to 5-HT and PGF2 alpha were inhibited by indomethacin, but those to KCl were not.
Arteries↗
A comparison of wax matrix and microencapsulated potassium chloride in relation to upper gastrointestinal illness requiring hospitalization.
The frequency of hospitalization for documented upper gastrointestinal illness among recipients of either wax matrix or microencapsulated potassium chloride was similar in a study in which clinics were randomly assigned to dispense one or the other preparation. The results indicate that there is no material difference between the two preparations in relation to serious upper gastrointestinal illness.
Adult↗
[Liberation of adenosine triphosphate after depolarization of the Torpedo electroplaque by potassium chloride].
The release of ATP after potassium depolarization was measured on fragments of electric tissue incubated in a solution containing the firefly extract. Light emission was proportional to the extracellular KCL concentration. In contrast to the release of ATP after single nerve impulses, the release after direct KCL depolarization was insensitive to curare of eserin.
Adenosine Triphosphate↗
Decrease of cardiac mass following excess dietary potassium chloride in the rat.
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Animals↗
[Inadvertent potassium chloride infusion in an epidural catheter].
In a 65 years old male patient 38 cc of a 7.45% potassium chloride-solution was inadvertently infused within 3 hours into an epidural catheter on the first postoperative day. The epidural potassium chloride administration resulted in a paresis and painful paraesthesia of the patient's legs and a level of sensory blockade to TH 11. Furthermore vegetative symptoms like hypertension and tachycardia were observed. For therapy a single bolus of 40 mg dexamethasone was administered intravenously followed by an epidural infusion of sodium chloride 0.9% 99 cc/h for several hours. About 6 hours after the start of infusion all symptoms had disappeared. It is proposed that the use of colour-coded epidural catheter devices and coloured electrolyte solutions as well as infusion-pumps with a larger reservoir that reduce the frequency of syringe changes would be helpful in avoiding such complications.
Aged↗
Clinical disorders of sodium, potassium, chloride, and sulfur metabolism. Diagnostic approach in children.
Information concerning normal concentrations of serum sodium, potassium, chloride, and sulfate as well as clinically useful data concerning absorption and excretion of these physiologically important ions are reviewed. Clinical approaches to diagnosis of these electrolyte disturbances are summarized with special emphasis on interpretation and treatment of some of these disorders in children.
Acute Kidney Injury↗
Effects of dexamethasone on sodium-potassium-chloride cotransport in trabecular meshwork cells.
PURPOSE: Previous studies in the authors' laboratory have shown that bovine and human trabecular meshwork (TM) cells possess a robust sodium-potassium-chloride (Na-K-Cl) cotransport system that functions in regulating intracellular volume and may play a central role in modulating outflow facility across the TM. Dexamethasone, which can induce ocular hypertension, has been found to increase resistance to aqueous outflow across the TM. The current study was conducted to investigate the hypothesis that alteration of TM cell Na-K-Cl cotransport function, regulation, or both may be an underlying factor in steroid-induced glaucoma. To this end, the authors evaluated the effects of dexamethasone treatment of TM cells on Na-K-Cl cotransport activity and cotransporter protein expression. METHODS: Cultured bovine and human TM cell monolayers were exposed to dexamethasone (10(-9) to 10(-6) M) for varying times, then evaluated for Na-K-Cl cotransport activity or harvested for cellular membrane proteins. Cotransport activity was assessed as bumetanide-sensitive K influx. Cotransport protein expression was evaluated by Western blot analysis of cellular proteins using a monoclonal antibody to the human colonic T84 epithelial cell Na-K-Cl cotransporter. RESULTS: The authors found that 24- and 48-hour exposures of human and bovine TM cells to dexamethasone stimulates Na-K-Cl cotransport activity (10(-8) to 10(-6) M dexamethasone in human cells; 10(-8) and 10(-7) M in bovine cells). The authors also found that dexamethasone (10(-8) M) stimulates Na-K-Cl cotransport activity of TM cells with exposure times as early as 12 hours and up to 5 days. In addition, the authors found that the level of Na-K-Cl cotransport protein expressed in TM cells is modulated by dexamethasone. When bovine or human TM cells are exposed to 10(-8) or 10(-6) M dexamethasone for 2 to 5 days, cotransporter protein expression is increased. With longer exposures, however, cotransporter protein levels decrease below control levels. Finally, the authors found that TM cells exposed to dexamethasone become unresponsive to regulation by hypertonicity and vasopressin. CONCLUSIONS: The authors' findings suggest that dexamethasone may be exerting its effect, at least in part, through altering Na-K-Cl cotransport function and regulation in TM cells.
Animals↗
Norepinephrine efflux evoked by potassium chloride in cat sympathetic nerves: dual mechanism of action.
Using a dialysis technique, prominent efflux of norepinephrine (NE) from cardiac sympathetic nerve endings was observed under local administration of potassium chloride (KCl, 100 mM). KCl induced NE efflux was suppressed by omega-conotoxin GVIA or desipramine but residual efflux of NE was still detectable. In the presence of omega-conotoxin GVIA, KCl induced efflux of NE was augmented by pretreatment with reserpine, indicating that this efflux of NE was derived from axoplasma with neurotransporter. These data suggest that a KCl induced brisk increase in dialysate NE levels might occur as a consequence of exocytotic NE release and carrier mediated outward NE transport from nerve endings.
Adrenergic Uptake Inhibitors↗