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At least 631 records · Page 35Linked to original sources
PubMed1977

[Paralysis, organic brain syndrome, and cardiac dysrhythmias caused by chronic laxative abuse (author's transl)].

A 39-year-old woman developed generalised paralysis, reversible organic brain syndrome, and cardiac dysrhythmias after 15 years of laxative abuse. Under continuous and cautious administration of potassium the cardiac rhythm became normal within four days and two days later the paralysis and organic brain syndrome almost disappeared. The cause of the psychiatric symptoms is thought to be cerebral potassium deficiency and an abnormal sodium/potassium equilibrium. Other clinical signs and symptoms due to extreme potassium depletion are presented. The importance of Na+/K+-activated membrane ATP-ase in myocardium and CNS is discussed.

Adult↗
PubMed2006

Behavioral motor dysfunction in Kv3-type potassium channel-deficient mice.

The voltage-gated potassium channels Kv3.1 and Kv3.3 are expressed in several distinct neuronal subpopulations in brain areas known to be involved in motor control such as cortex, basal ganglia and cerebellum. Depending on the lack of Kv3.1 or Kv3.3 channel subunits, mutant mice show different Kv3-null allele-dependent behavioral alterations that include constitutive hyperactivity, sleep loss, impaired motor performance and, in the case of the Kv3.1/Kv3.3 double mutant, also severe ataxia, tremor and myoclonus (Espinosa et al. 2001, J Neurosci 21, 6657-6665, Genes, Brain Behav 3, 90-100). The lack of Kv3.1 channel subunits is mainly responsible for the constitutively increased locomotor activity and for sleep loss, whereas the absence of Kv3.3 subunits affects cerebellar function, in particular Purkinje cell discharges and olivocerebellar system properties (McMahon et al. 2004, Eur J Neurosci 19, 3317-3327). Here, we describe two sensitive and non-invasive tests to reliably quantify normal and abnormal motor functions, and we apply these tests to characterize motor dysfunction in Kv3-mutant mice. In contrast to wildtype and Kv3.1-single mutants, Kv3.3-single mutants and Kv3 mutants lacking three and four Kv3 alleles display Kv3-null allele-dependent gait alterations. Although the Kv3-null allele-dependent gait changes correlate with reduced motor performance, they appear to not affect the training-induced improvement of motor performance. These findings suggest that altered cerebellar physiology in the absence of Kv3.3 channels is responsible for impaired motor task execution but not motor task learning.

Animals↗
PubMed1980

Role of water balance in the enhanced potassium excretion and hypokalaemia of rats with diabetes insipidus.

1. The role of water balance in the hypokalaemia of rats with diabetes insipidus (DI rats) was studied. 2. After a 3-day balance study DI rats had a lower muscle potassium content, and plasma [K+], and the urinary excretion of potassium in response to oral KCl loading was reduced when compared to normal rats. The hypokalaemia was found to be associated with elevated concentrations of potassium in renal medulla and papilla when compared to values in normal Long-Evans rats. 3. During a 9-day balance study urinary potassium excretion was higher than that of normal rats on days 1-3, but not different on days 4-9; this transient elevation was observed in DI rats on normal, high and low potassium diets. On a low potassium diet the urinary potassium excretion of DI rats fell to minimal levels, making unlikely the existence of a renal defect in potassium handling. 4. Muscle potassium content and plasma [K+] were normal after 9 days in metabolism cages. This spontaneous reversal of the hypokalaemia of DI rats was associated with increased water content of renal medulla and papilla, and decreased potassium concentration in these zones. 5. The effect of acute mild dehydration on potassium handling of DI rats was evaluated. Water deprivation for 1-8 hr was sufficient to raise the urinary potassium excretion of DI rats above that of DI rats drinking ad lib. Renal tissue [K+] was significantly increased after 8 hr of dehydration. Water deprivation also enhanced the response of DI rats to an oral KCl load. Two days of chronic dehydration in the form of water rationing also significantly enhanced the urinary potassium excretion of DI rats. 6. These data suggest that chronic mild dehydration may be responsible for the modest potassium deficiency observed in DI rats via alterations in renal tissue [K+] and consequently in urinary potassium excretion. Correction of dehydration during prolonged periods in metabolism cages may account for the spontaneous reversal of the hypokelaemic condition.

Animals↗
PubMed1979

Na,K-ATPase in excitation-contraction coupling of vascular smooth muscle from cattle.

Lowering the extracellular K+ content from 6 to 0.6 mM causes a rise, and elevation from 6 to 8.5 mM a fall of 45Ca++ efflux from the vascular smooth muscle cells of the arteria carotis communis of cattle. In contrast, a level of 17 mM K+ has no influence. Removal of extracellular calcium does not block these effects. 10(-4) M ouabain also induces a rise in Ca++ efflux, additional potassium reduction then being without effect; 10(-9) M ouabain is of no influence. The 45Ca++ efflux kinetics correlates with the activity of the isolated Na,K-ATPase. Tonus increases of the vascular strips by 10(-4) M ouabain and potassium deficiency cannot be blocked by 4 mM lanthanum or removal of extracellular calcium. Unlike sodium, potassium stimulates the active Ca++ binding and the activity of the Ca-ATPase of the microsomal fraction. The ative Ca++ binding of the mitochondria is stimulated by both ions. It is postulated that the activity of the plasma membrane Na,K-pump is able to regulate the tonus of big arteries through alteration of Ca++ storage processes.

Animals↗
PubMed1982

The effects of antidiuretic hormone and state of potassium balance on the renin-angiotensin system in rats with diabetes insipidus.

1. The influence of ADH and the state of potassium balance on the renin-angiotensin system was studied in rats with hereditary diabetes insipidus (DI rats). 2. Plasma renin concentration in DI rats was higher than in control Long-Evans rats. 3. Spontaneous reversal of the hypokalaemia normally found in DI rats did not reduce plasma renin concentration (p.r.c.), suggesting that potassium deficiency does not contribute significantly to the elevation of p.r.c. in DI rats. Similarly, a low potassium diet failed to further increase p.r.c. in DI rats. 4. In contrast, the p.r.c. of DI rats was significantly diminished by a high potassium intake both in the presence and absence of ADH. A highly significant inverse correlation was found between p.r.c. and urinary potassium excretion in both ADH-treated and untreated DI rats on low, normal and high potassium diets. 5. Plasma renin concentration was significantly lower in ADH-treated than in untreated DI rats on a high potassium intake, suggesting that the inhibitory effects of ADH and potassium are additive. 6. ADH consistently reduced p.r.c. in DI rats independent of the state of potassium balance. 7. ADH and potassium may inhibit renin secretion via different mechanisms of action.

Animals↗
PubMed1989

Potassium depletion and regulation of angiotensin II receptors in vascular smooth muscle cells.

Mesenteric artery smooth muscle cells were grown in culture media containing high, normal, or low concentrations of potassium to study the effects on angiotensin II (Ang II) receptor regulation. Cell growth was similar among cells grown in the different culture media. Cells grown in high potassium media (K = 5.8 mEq/L) had an equilibrium dissociation constant, Kd, of 1.59 +/- 0.2 nM, whereas those grown in normal potassium media (K = 4.1 mEq/L) had a Kd of 1.79 +/- 0.2 nM and those grown in a low potassium media (K = 2.9 mEq/L) had a Kd of 1.19 +/- 0.12 nM (not significantly different, NS). Binding capacity of smooth muscle cells grown in high potassium media was 81 +/- 16.7 fmol/mg prot, 95.1 +/- 12.4 fmol/mg prot in those grown in normal potassium media and those grown in low potassium media 86.4 +/- 24.1 fmol/mg prot (NS). Binding of radiolabelled Ang II was reduced by approximately 70% in cells exposed to unlabelled Ang II for 30 or 60 minutes. However, this effect of exposure to Ang II to reduce subsequent binding of Ang II was identical in cells grown in high and low potassium medium. Therefore, we were unable to identify a direct effect of low potassium to induce changes in Ang II receptor binding affinity or binding capacity. Previously observed changes in these Ang II binding parameters in potassium-depleted rats was probably a consequence of other factors which were simultaneously altered by potassium deficiency.

Angiotensin II↗
PubMed1983

Pathogenesis of arrhythmogenic changes due to magnesium depletion.

Magnesium and potassium deficiency may complicate prolonged treatment with any diuretic causing hypermagnesiuria and hyperkaliuria. Hypomagnesaemia is usually associated with reduced intracellular magnesium and potassium levels and increases in sodium and cytosolic calcium concentrations within the myocardium. These changes give rise to nonspecific clinical signs and symptoms. No satisfactory routine procedure exists for the evaluation of total body magnesium levels.

Arrhythmias, Cardiac↗
PubMed1976

High sodium-low potassium environment and hypertension.

The high sodium-low potassium environment of civilized people, operating on a genetic substrate of susceptibility, is the cardinal factor in the genesis and perpetuation of "essential" hypertension. The noxious effects begin in childhood, when habits of excess salt consumption are acquired at the family table, and are perpetuated by continuing habit and by increasing use of convenience and snack foods with artificially high concentrations of sodium and low levels of potassium. Present methods of food preparation leach out the protective potassium. Extradietary sodium chloride is a condiment not a requirement. Some primitive populations clearly preferred potassium chloride to sodium chloride. Chronic expansion of extracellular fluid volume induced by excess salt consumption causes the central and peripheral circulatory regulatory mechanisms to work at cross purposes, resulting in increased arterial pressure. The protective effect of potassium is dramatic and easily demonstrable in animals and man but its mechanism is not known. It cannot be entirely a direct effect on blood pressure because rats protected with extra potassium against a moderately high salt intake live much longer than control rats but have the same elevated blood pressures. In hypertension with a demonstrable "cause," the high sodium-low potassium environment makes a bad matter worse. In nature, feral man and his forebears were not confronted with excessive sodium and deficient potassium; indeed, the reverse was the case. Evolution has provided powerful mechanisms for conserving sodium and eliminating potassium, but no efficient physiologic mechanisms for conserving potassium and eliminating excess sodium. Most laboratory animal "control" diets contain an amount of sodium that fully suppresses aldosterone secretion, and the same is true of the "average" diet of the American people. Inadequate attention to dietary sodium and potassium makes many studies in both animals and man of uncertain validity. Internally, essential hypertension is an exceedingly complex mosaic of physiologic interactions. Viewed from outside, it is a disorder for which genetic material sets the stage; excessive sodium precipitates it and perpetuates it. Extra salt makes all forms more rapidly progressive and accelerates the onset of terminal events; extra potassium is everywhere protective. When an entire population eats excessively of salt, hypertension will develop among those genetically susceptible, but epidemiologic studies of salt versus blood pressure will not show a relation of salt to hypertension. This is the saturation effect. Low sodium diets are therapeutically effective but generally regarded as an impossible or an unnecessary nuisance. Effective prevention programs must be instituted at as early an age as possible. The efficacy of a prophylactic/therapeutic low sodium-high potassium diet should be weighed against the uncertain hazards of a lifetime of pill taking.

Adolescent↗
PubMed1972

Translocation of carbon-14 in sugarcane plants supplied with or deprived of phosphorus.

Translocation of radioactive carbon from the fed part of a blade to the rest of the plant was impaired by a deficiency in phosphorus only when the level of phosphorus was low enough to decrease growth.Phosphorus deficiency decreased the percentage of inorganic phosphorus more than that of organic phosphorus, indicating little effect of phosphorus deficiency upon phosphorylation.Thus phosphorus deficiency did not reduce phosphorylation enough to affect translocation. Evidence for the involvement of phosphorylation in translocation obtained from studies with potassium deficiency, light intensity and quality, 3-(p-chlorophenyl)-1, 1-dimethylurea and 3-(3,4-dichlorophenyl)-1, 1-dimethylurea, and carbon dioxide suggests that noncyclic photosynthetic phosphorylation provides the energy for phototranslocation.

Journal Article↗
PubMed1978

Total body and exchangeable potassium in chronic airways obstruction: a controversial area?

Potassium deficiency is an important complication in the treatment of heart disease. However, there is a serious dichotomy in the literature. Severe potassium depletion has been reported in this condition when exchangeable potassium was measured whereas normal levels or marginal depletion were found in measurements of total body potassium. To clarify this situation, simultaneous measurements of total body potassium by whole-body counting, and of exchangeable potassium by isotope dilution using 43K, were made in 10 male subjects with established airways obstruction. Sequential determinations showed that exchangeable potassium increased up to 68 hours after administration, and values obtained at only 24 hours would have been a substantial underestimate. In this group of subjects neither total body nor exchangeable potassium at 48 hours was significantly different from the expected normal value.

Aged↗
PubMed2006

Expression profiling of the 14-3-3 gene family in response to salt stress and potassium and iron deficiencies in young tomato (Solanum lycopersicum) roots: analysis by real-time RT-PCR.

UNLABELLED: BACKGROUND AND AIMS Mineral nutrient deficiencies and salinity constitute major limitations for crop plant growth on agricultural soils. 14-3-3 proteins are phosphoserine-binding proteins that regulate the activities of a wide array of targets via direct protein-protein interactions and may play an important role in responses to mineral nutrients deficiencies and salt stress. In the present study, the expression profiling of the 14-3-3 gene family in response to salt stress and potassium and iron deficiencies in young tomato (Solanum lycopersicum) roots was investigated in order to analyse the 14-3-3 roles of the proteins in these abiotic stresses. METHODS: Sequence identities and phylogenetic tree creation were performed using DNAMAN version 4.0 (Lynnon Biosoft Company). Real-time RT-PCR was used to examine the expression of each 14-3-3 gene in response to salt stress and potassium and iron deficiencies in young tomato roots. KEY RESULTS: The phylogenetic tree shows that the 14-3-3 gene family falls into two major groups in tomato plants. By using real-time RT-PCR, it was found that (a) under normal growth conditions, there were significant differences in the mRNA levels of 14-3-3 gene family members in young tomato roots and (b) 14-3-3 proteins exhibited diverse patterns of gene expression in response to salt stress and potassium and iron deficiencies in tomato roots. CONCLUSIONS: The results suggest that (a) 14-3-3 proteins may be involved in the salt stress and potassium and iron deficiency signalling pathways in young tomato roots, (b) the expression pattern of 14-3-3 gene family members in tomato roots is not strictly related to the position of the corresponding proteins within a phylogenetic tree, (c) gene-specific expression patterns indicate that isoform-specificity may exist in the 14-3-3 gene family of tomato roots, and (d) 14-3-3 proteins (TFT7) might mediate cross-talk between the salt stress and potassium and iron-deficiency signalling pathways in tomato roots.

14-3-3 Proteins↗
PubMed1988

Magnesium, potassium and zinc deficiency in subjects with type II diabetes mellitus.

The concentrations of magnesium, potassium and zinc were determined in plasma, erythrocytes, muscle biopsies, and in urine collected during 24 hours, in 18 subjects with type II diabetes mellitus (DM). Magnesium was also determined in mononuclear cells. The results were compared with those in 35 (magnesium and potassium analyses) or 26 (zinc analyses) healthy controls. Subjects with type II DM had lower concentrations of magnesium (3.79 +/- 0.32 vs. 4.29 +/- 0.22 mmol/100 g FFDS), potassium (40.5 +/- 5.17 vs. 46.1 +/- 3.81 mmol/100 g FFDS) and zinc (231 +/- 29 vs. 247 +/- 23 ng/mg FFDS) in skeletal muscle. Furthermore, the urinary excretions of magnesium and zinc were higher, as compared with those in healthy controls (5.00 +/- 2.68 vs. 3.62 +/- 1.47 mmol/24 hours, and 683 +/- 285 vs. 326 +/- 205 micrograms/24 hours, respectively). The contents of magnesium, potassium and zinc plasma did not correlate with the corresponding concentrations in skeletal muscle or circulating blood cells, as investigated in healthy controls, diabetics and in all subjects together, implying that the plasma concentrations are not useful in the assessment of electrolyte status. Hence, deficiency of electrolytes frequently occurs, and should be looked for, in subjects with type II DM.

Adult↗
PubMed1995

[Indications for the use of magnesium in anesthesia and intensive care].

Magnesium (Mg), a cofactor in numerous enzymatic reactions, is often ignored by clinicians, as the symptomatology of Mg depletion is not specific and usually associated with that of the cause of the depletion. Furthermore, the plasma Mg concentration (0.8 to 1.1 mmol.L-1) is only equivalent to one percent of the total body content. A Mg deficit may exist while plasma Mg concentration is normal. Therefore other techniques for Mg assessment, such as the repletion test, as well as red blood cell and lymphocyte concentrations have been used. A renewed interest for Mg occurred as numerous studies have shown the therapeutic efficiency of Mg and as the mechanisms of its haemodynamic effects have been recognized. Mg regulates Na-K-ATPase activity, K channels activity and, most of all, it is a natural calcium channel blocking agent. These properties explain its important place in electrophysiology of myocardial cells and the effects on the tension of smooth muscles, resulting in a vasodilation and a bronchodilation respectively. The antagonistic effect of Mg on calcium decreases the presynaptic release of acetylcholine at the neuromuscular junction and the release of epinephrine at the peripheral sympathetic nerves and the adrenals. Mg potentiates the effect of non-depolarizing muscle relaxants. A Mg deficiency occurs often in ICU patients, in alcoholics and during use of diuretics. Simultaneous administration of Mg is often required for treatment of potassium deficiency. Mg has an anti-arrhythmic effect towards digoxin-mediated dysrhythmias and torsades de pointes, and can be efficient in other arrhythmias. Systematic use of Mg seems to decrease mortality of acute myocardial infarction and is justified during cardiac surgery, often associated with hypomagnesemia, because of vasodilation of coronary arteries and in order to prevent occurrence of arrhythmias. Mg, because of its calcium channel blocking properties and as it lowers the release of epinephrine, is indicated for surgery of pheochromocytoma. In eclamptic and pre-eclamptic patients, the use of Mg is valuable, but not as an anti-epileptic agent. Other clinical uses of Mg have been proposed, but they are either anecdotal or of uncertain efficiency.

Anesthesia↗
PubMed1998

Hypokalemia alters sex hormone and gonadotropin levels: evidence that FSH may be required for luteinization.

Hypokalemia produced different effects on steroid sex hormone concentrations in plasma and ovary in the mouse. Estradiol levels were slightly increased, whereas circulating progesterone was markedly decreased in all estrous periods. The preovulatory surge of gonadotropins and the secondary surge of follicle-stimulating hormone (FSH) at estrus were also decreased, but basal levels of both gonadotropins were unaffected. Supplementation with luteinizing hormone (LH), FSH, or gonadotropin-releasing hormone (GnRH) at proestrus rapidly normalized plasma and ovarian progesterone levels at this stage of the estrous cycle. Plasma progesterone levels at diestrus were restored only by combined treatment, at the periovulatory stage, with LH and FSH or GnRH but not by LH or FSH alone. The results demonstrate a lack of steroidogenic activity in the corpus luteum of the potassium-deficient mice and, furthermore, that FSH plays an important role in luteinization in the hypokalemic mice. We conclude that alteration of the transcellular potassium gradient may affect the regulation of the periovulatory surge of gonadotropins and progesterone secretion, probably by altering the release of GnRH from the hypothalamus. In addition, the results suggest that FSH may play a certain role as a luteotropic hormone in mice.

Animals↗
PubMed1984

Effects of desoxycorticosterone acetate on magnesium metabolism in potassium-depleted rats.

Metabolic balance studies were performed in two groups of 6 rats each, pair-fed a diet deficient in potassium. While one group was injected with desoxycorticosterone acetate (DOCA) for 11 days, the other group, used as a control, was injected with oil. The administration of DOCA suppressed or reversed the thirst, natriuresis, diuresis, calciuria and magnesiuria that developed in the potassium-deficient control group. Potassium-depleted DOCA-treated rats had a more positive water and sodium balance, experienced a significant expansion in plasma volume, had a more negative potassium balance and had a lower plasma potassium concentration. Magnesium balance decreased in the group fed the diet deficient in potassium and injected with oil but it rose towards control levels in the group fed the same diet and treated with DOCA. As the content of potassium in muscle decreased in rats fed the diet deficient in potassium and injected with oil, the concentration of magnesium in muscle also fell and the plasma concentration of magnesium increased. Thus, the hypermagnesemia of potassium depletion could be explained by the shifting of magnesium from tissue into the extracellular space. The partial compensation of the hypermagnesemia observed in the potassium-deficient group injected with DOCA may be the result of the hemodilution secondary to plasma expansion.

Animals↗
PubMed1996

[Bartter's syndrome. A condition with chronic hypokalemia].

Bartter's syndrome (BS) is a disease with severe hypokalaemia due to renal potassium wasting. The potassium loss is due to lesions at different sites within the renale tubule. Additional features include metabolic alkalosis, excess renal production of prostaglandins, hyperreninaemia, hyperaldosteronism and impaired pressor responses to exogenous angiotensin II. These secondary features are the result of renal potassium wasting. Symptoms are due to potassium deficiency, but many adult patients feel well despite marked hypokalaemia. The hypocalciuric variant of BS is called Gitelman's syndrome. These patients have a more benign course. The diagnosis of BS is one of exclusion, mainly of surreptitious vomiting, diuretic or laxative abuse. The primary treatment is potassium supplementation often in combination with potassium-sparing diuretics, prostaglandin inhibitors or ACE-inhibitors. With coexisting magnesium deficiency, magnesium supplementation might be effective.

Adult↗
PubMed1982

Captopril in the management of hypertension with renal artery stenosis: its long-term effect as a predictor of surgical outcome.

Fifteen patients with hypertension and unilateral renal artery disease were treated with captopril alone; 10 came to operation and were later assessed postoperatively with no drug treatment. Captopril caused both immediate and sustained decreases in plasma angiotensin II and aldosterone, with increases in plasma active renin and blood angiotensin I concentrations. Decrements in systolic and diastolic pressure 2 hours after the first dose of captopril were closely correlated with the initial decreases in plasma angiotensin II. Blood pressure was decreased by long-term captopril therapy irrespective of whether plasma angiotensin II was abnormally high before treatment. The long-term response of both systolic and diastolic pressure correlated well with the response to surgery. By contrast, the blood pressure decrease 2 hours after the initial dose of captopril variously underestimated and overestimated the decrease during prolonged use of the drug and did not relate to surgical outcome. In patients who, before treatment, had secondary aldosteronism, hyponatremia, hypokalemia and sodium and potassium deficiency, captopril corrected these abnormalities. In the remaining patients, long-term captopril therapy did not alter exchangeable sodium, plasma sodium or total body potassium, although plasma potassium levels increased.

Adolescent↗