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At least 145 records · Page 8Linked to original sources
PubMed1990

Effects of lead and a low-molecular-weight endogenous plasma inhibitor on the kinetics of sodium-potassium-activated adenosine triphosphatase and potassium-activated p-nitrophenylphosphatase.

1. Lead, ouabain and an endogenous plasma inhibitor were all found to be potent inhibitors of purified hog cerebral cortex sodium-potassium-activated adenosine triphosphatase and potassium-stimulated p-nitrophenyl-phosphatase. 2. The kinetic characteristics of inhibition of both enzymes by lead and the endogenous plasma inhibitor differed in several respects. For sodium-potassium-activated adenosine triphosphatase, lead and the endogenous plasma inhibitor were non-competitive inhibitors with respect to potassium; lead was competitive with respect to sodium, whereas the endogenous plasma inhibitor had no effect; lead was competitive with respect to magnesium adenosine triphosphate, whereas the endogenous plasma inhibitor was uncompetitive. For potassium-activated p-nitrophenylphosphatase, both lead and the endogenous plasma inhibitor were competitive with respect to potassium; lead showed a mixed type of inhibition with respect to p-nitrophenylphosphate, whereas the endogenous plasma inhibitor was non-competitive. 3. Lead and the endogenous plasma inhibitor exhibited synergistic inhibitory activity on sodium-potassium-activated adenosine triphosphatase. 4. These results suggest that lead could play a contributory role in the pathogenesis of essential hypertension via an additive inhibition of vascular smooth muscle sodium-potassium-activated adenosine triphosphatase.

4-Nitrophenylphosphatase↗
PubMed1975

Potassium metabolism in patients with rheumatoid arthritis. Effects of treatment with depot tetracosactrin, spironolactone, and oral supplements of potassium chloride.

(1) Plasma and urine electrolytes and whole body potassium have measured before and after a 2-week administration of depot tetracosactrin 0.5 mg on alternate days to eight patients with rheumatoid arthritis (RA.) The effects of adding supplements of potassium chloride (48 mmol/d) and spironolactone 200 mg daily have been investigated. (2) Acute changes in red blood cell water and potassium content, plasma electrolyte concentration, and plasma 11-hydroxycorticosteroid levels were measured for 48 hours after a single intramuscular injection of 0.5 mg depot tetracosactrin in six patients with RA. (3) The measured total body potassium was significantly less than that predicted from the height, weight, and age formula in patients with RA. (4) Treatment with depot tetracosactrin resulted in an acute fall in plasma and red cell potassium independent of external potassium loss. (5) Two weeks of treatment with depot tetracosactrin resulted in hypokalaemia and a rise in plasma sodium and bicarbonate. There was no associated electrocardiogram changes or a rise in blood pressure. (6) Neither oral potassium supplements nor spironolactone altered total body potassium. (7) The significance of the findings and the physiological mechanisms underlying them are discussed.

Adult↗
PubMed1980

Renal potassium adaptation: Na-K-ATPase activity along the nephron after chronic potassium loading.

To identify nephron sites where renal potassium adaptation takes place, Na-K-ATPase was measured with a micromethod along the nephron of potassium-loaded mice. A possible role of aldosterone in this process was evaluated in K-loaded animals treated concurrently with pharmacologic doses of spironolactone. Animals fed a potassium-enriched diet for at least 2 wk excreted about 90% of ingested potassium in the urine, and fractional potassium clearance averaged 87 +/- 8%, compared with 13 +/- 2% in controls. Na-K-ATPase activity per millimeter tubule length increased by 225% in the cortical collecting tubule and by 177% in the medullary collecting tubule, but was not substantially affected in other nephron segments. Stimulation of Na-K-ATPase was identical in the cortical collecting tubule of K-loaded mice treated with spironolactone. These results indicate that chronic potassium loading in the mouse results in an adaptive increase potassium loading in the mouse results in an adaptive increase in Na-K-ATPase in the collecting tubule and suggest that this nephron segment is the major site of potassium adaptation in this species. This effect appears to be independent of aldosterone.

Adenosine Triphosphatases↗
PubMed1998

Reappraisal of the quantity and nature of renal calcifications and mineral metabolism in the magnesium-deficient rat. Effects of treatment with potassium citrate or the combination magnesium citrate and potassium citrate.

There is an urgent need for drugs capable of inhibiting renal calcifications, nephrocalcinosis and stones included, in humans. Current anticalcification medication is based mainly on alkalinization of the metabolism using potassium-containing citrate alone, despite the fact that calcium stone patients suffer marginally from both magnesium and potassium deficiency. We investigated the anticalcification efficacy of oral potassium citrate versus the combined administration of this drug and magnesium citrate in the magnesium-deficient rat developing corticomedullary nephrocalcinosis and luminal microliths in the long term. Among other things we employed specific stains for calcium and oxalate, light microscopy and element analysis for renal tissue and calcifications, respectively. In addition, minerals in renal tissue, urine and plasma were determined, as well as the state of extracellular calcium homeostasis. Magnesium deficiency caused pure calcium phosphate tissue deposits, containing no magnesium, but no deposition of calcium oxalate in the tubular lumen; tissue magnesium, calcium and phosphorus were increased, and there was marked potassium wastage via urine; despite mild hypercalcemia other signs of hyperparathyroidism were not found. Alkalinization with the two kinds of medication evoked an increase in urinary pH, citrate, and potassium; however, potassium citrate alone tended to aggravate renal concretions, whereas the combination of this drug with magnesium citrate completely prevented concretions. It was concluded that: (1) magnesium deficiency-induced calcifications are oxalate-free and are not sensitive to mobilization by alkalinization with potassium citrate, which might explain the failure of the drug to prevent stone recurrence in clinical stone patients, and (2) the combination of potassium citrate and magnesium citrate, which shows enormous anticalcification efficacy, deserves high priority in clinical trials aimed at evaluating strategies for the prevention of stones.

Animals↗
PubMed2004

Lack of genotoxicity of potassium iodate in the alkaline comet assay and in the cytokinesis-block micronucleus test. Comparison to potassium bromate.

Iodine could be added to the diet of human population in the form of iodide or iodate but iodate had not been adequately tested for genotoxicity and carcinogenicity. In the present study, genotoxic effects of potassium iodate were evaluated in vitro using the alkaline comet assay and the cytokinesis-block micronucleus assay on CHO cells and compared to halogenate salt analogues potassium bromate and chlorate and also to their respective reduced forms (potassium iodide, bromide and chloride). The results showed that the comet assay failed to detect the presence of DNA damage after a treatment of cells by potassium iodate for concentrations up to 10 mM. This absence of primary DNA damage was confirmed in the cytokinesis-block micronucleus assay. In the same way, results showed that potassium chlorate as well as potassium iodide, bromide and chloride did not induced DNA damage in the alkaline comet assay for doses up to 10 mM. By contrast, potassium bromate exposure led to an increase in both DNA damage and frequency of micronucleated cells. The repair of bromate-induced DNA damage was incomplete 24 h after the end of treatment. These results seem to indicate that potassium bromate would induce DNA damage by several mechanisms besides oxidative stress.

Animals↗
PubMed1993

[Potassium substitution during coronary surgery: K(+)-Mg+(+)-aspartate-complex (Inzolen) versus potassium chloride].

Potassium loss may cause arrhythmias and cardiac injury in patients undergoing heart surgery with cardiopulmonary bypass (CPB). In a prospective, randomized trial two different methods of potassium substitution were investigated regarding their influence on cardiac rhythm following reperfusion. Patients received either potassium chloride (Group I, n = 102) or potassium magnesium aspartate (Inzolen, group II, n = 105) to achieve intraoperative serum potassium concentrations of 4.5 mmol/l. St. Thomas cardioplegic solution was used. CPB was performed in moderate hypothermia (28-32 degrees C) with a non-pulsatile pump flow, a membrane oxygenator and a single two-stage venous catheter. The two study groups were comparable with regard to biometric data, preoperative state, duration of operation, ischemia and clinical outcome. In 6 patients in group I and in 3 patients in group II perioperative myocardial infarction was diagnosed based on ECG and CK-MB findings. One patient in each group died during the postoperative hospital stay. At the time of declamping mean serum potassium concentration was 4.9 +/- 0.7 mmol/l in group I and 4.8 +/- 0.5 mmol/l in group II (n.s.). The concentration of magnesium was significantly lower in the potassium chloride substitution group (1.48 mmol/l) compared to the other group (2.33 mmol/l) (p < 0.05). No significant differences in cardiac electric activity were observed between the two groups. The incidence of ventricular fibrillation in the early reperfusion period was 37% versus 45% (n. s.). In both groups patients with a potassium value of < 4.5 mmol/l showed a significantly higher incidence of ventricular fibrillation. Five percent of the patients had bradycardia requiring temporary pacing.(ABSTRACT TRUNCATED AT 250 WORDS)

Aspartic Acid↗
PubMed1974

Total body potassium in long-term frusemide therapy: is potassium supplementation necessary?

Measurements of total body potassium (T.B.K.) were made by whole-body counting in four groups of patients receiving oral frusemide for one year. Patients in group 1 had essential hypertension and normal renal function and received 40 mg frusemide daily without potassium supplements. Patients in group 2 were similar but received oral potassium supplements for the first four months of treatment. Patients in group 3 had hypertension associated with renal disease and received 120 mg frusemide daily without potassium supplements. Patients in group 4 also had hypertension and renal impairment and in addition to 120 mg frusemide daily they received oral potassium supplements for four months. No evidence of depletion of T.B.K. was found in any of the groups after continuous treatment with frusemide for one year. It is questioned whether potassium supplementation in long term diuretic therapy with frusemide is necessary unless there is evidence of pre-existing potassium depletion or of some other factor such as cardiac failure, cirrhosis of the liver, or the nephrotic syndrome.

Administration, Oral↗
PubMed1999

Comparative evaluation of the genotoxic properties of potassium bromate and potassium superoxide in V79 Chinese hamster cells.

The genotoxic potential of two oxidizing compounds, potassium bromate and potassium superoxide, was comparatively tested in various genotoxicity tests with V79 Chinese hamster cells. Both substances clearly induced cytotoxicity, chromosome aberrations and increased DNA migration in the alkaline comet assay. Using a modified comet assay protocol with FPG protein, a DNA repair enzyme which specifically nicks DNA at sites of 8-oxoguanines and formamidopyrimidines, we detected oxidative DNA base damage only after potassium bromate treatment. HPLC analysis also revealed significantly increased levels of 8-oxodeoxyguanosine after potassium bromate treatment but not after potassium superoxide treatment. Furthermore, potassium bromate clearly induced gene mutations at the HPRT locus while potassium superoxide only had a small effect on HPRT mutant frequencies. Molecular analysis of potassium bromate-induced mutations indicated a high portion of deletion mutations. Three out of four point mutations were G to T transversions which typically arise after replication of 8-oxoguanine. Our results suggest that the two oxidizing compounds induce specific patterns of genotoxic effects that reflect the types of DNA alterations induced by different reactive oxygen species (ROS).

8-Hydroxy-2'-Deoxyguanosine↗