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At least 253 records · Page 14Linked to original sources
PubMed1991

Potassium channels and epilepsy: evidence that the epileptogenic toxin, dendrotoxin, binds to potassium channel proteins.

Dendrotoxin-I, a component of the venom of the black mamba snake, Dendroaspis polylepsis, was used to affinity purify a potassium channel from bovine brain. This dendrotoxin-I binding protein was composed of several subunits with molecular weights of 35,000, 38,000, 42,000 and 74,000. Partial sequence resulting from Edman degradation of the N-terminus of the 74 kDa subunit was identical to the predicted amino acid sequence of the N-terminus of a protein encoded by a mouse/rat homologue of the Shaker gene family of potassium channels, MK2/RBK2 (RCK5). Polyclonal antibodies raised against synthetic peptides derived from the predicted amino acid sequence of another member of this family, MK1, recognized this 74 kDa subunit. Due to extensive amino acid sequence identity between MK2 and MK1, it is likely that antibodies recognized epitopes common to both. Thus, from an immunological standpoint, either MK1, MK2, or both channel proteins could have been present in this 74 kDa band on protein blots. Closely related K+ channels in bovine brain could have copurified based on their affinity for dendrotoxin-I (DTX-I). DTX-I was shown to inhibit MK1 currents in a time and voltage independent fashion. Physiological and molecular evidence indicates the existence of many types of DTX sensitive potassium channels in the mammalian brain, however, our protein sequencing of the 74 kDa subunit has detected the presence of only one unique N-terminal sequence, identical to MK2. The possible reason for the appearance of this discrepancy is discussed. This paper represents the first report identifying one dendrotoxin binding protein in bovine brain tissue (BK2) as a delayed rectifier type of potassium channel.

Amino Acid Sequence↗
PubMedDate not supplied

[Treatment of extreme hyperkalemia caused by diabetic ketoacidosis, potassium-sparing diuretics and potassium substitutes].

Grave hyperkalemic is a serious metabolic disorder. Its treatment fell into the fields of urgent medicine because of the risk of malignant cardiac arrhythmias that can be fatal for the patient. The article deals with the treatment of a 49-year-old female patient with decompensated liver cirrhosis and diabetes mellitus in whom grave hyperkalemia (9 mmol/1) with typical electrocardiographic changes was provoked by potassium saving diuretics combined with furosemide and the additional potassium substituted drugs, as well as development of diabetic ketoacidosis. Thanks to intensive medicinal treatment and constant follow-up of the patient rapid disappearance of hyperkalemia and ketoacidosis was observed. The success of medicinal therapy can be expected in cases of extreme hyperkalemia and relative hypokaliaemia. Intracellular hyperkaliaemia must be treated, without delay, with dialysis. Potassium saving diuretics and furosemide do not require additional potassium drugs, especially in risk patients in whom hyperkalemia may develop because of other existing diseases.

Acute Disease↗
PubMed1987

[Effect of extracellular potassium ions on the potassium outward current which depends on extracellular calcium ions].

Changes in the delayed potassium outward current induced by introduction of K+ ions into extracellular solution have been studied in experiments on isolated intracellularly perfused Helix neurons. It is shown that extracellular administration of 5-10 mmol/l K+ ions into the solution produces a reversible increase of the potassium outward current which depends on the extracellular Ca2+ ions (IK(Ca out)). Extracellular potassium increases this component of the potassium current as a result of weakening of its inactivation.

Animals↗
PubMed1989

Anti-ischemic effects of the potassium channel activators pinacidil and cromakalim and the reversal of these effects with the potassium channel blocker glyburide.

The direct cardioprotective efficacy of the potassium channel activators pinacidil and cromakalim was determined in isolated globally ischemic rat hearts. Isolated buffer-perfused rat hearts were subjected to 25 min of ischemia followed by 30 min of reperfusion. These hearts were pretreated with 1 to 100 microM pinacidil, 1 to 7 microM cromakalim or vehicle. Pinacidil resulted in significant improvements in reperfusion function and cardiac compliance, though it did not significantly reduce lactate dehydrogenase release at any concentration. The protective effects of pinacidil were greatest at a 10 microns concentration and were slightly diminished at higher concentrations (30 and 100 microns). Although not affecting the severity of ischemia alone, 10 microM glyburide (potassium channel blocker) completely reversed the protective effects of pinacidil on reperfusion function and compliance. Cromakalim (7 microM) resulted in a greater than 50% improvement in reperfusion function and compliance and unlike pinacidil significantly reduced lactate dehydrogenase release by approximately 50%. At 1 microM, glyburide alone did not significantly affect the severity of ischemia but reversed the protective effects of cromakalim. Not only did glyburide reverse the protective effects of cromakalim, it resulted in a worsening of ischemia compared to vehicle, an effect not seen with glyburide alone. Thus, both pinacidil and cromakalim appear to have direct cardioprotective efficacy, though some differences between them may be possible. The mechanism of their protective effects appears to be via potassium channel opening as the potassium channel blocker glyburide reverses the protective effect of these compounds. Intracellular electrophysiological studies showed that ischemia-induced depolarization was reversed with cromakalim, which increased the resting potential nearly back to preischemic levels.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

The effects of cetrimide and potassium bromate on the potassium ion concentration in the inner ear fluid of the guinea-pig.

The mammalian inner ear is located deep within the temporal bone. The organ of Corti, the delicate sensory system for sound, is surrounded by two fluid systems; the potassium-rich endolymph and the sodium-rich perilymph. The pathogenesis of inner ear deafness is thought to be largely due to an imbalance of potassium and sodium ions in the inner ear fluids. Dynamic changes in K+ in the endolymph and perilymph were studied in the guinea-pig following cetrimide (cetrimonium bromide, a powerful cationic detergent which shows ototoxicity) applications on the round window membrane, intramuscular injection of potassium bromate (bread whitener, known to cause renal damage and permanent deafness in animals and man). Maximum fall in K+ concentration in the endolymoh (mM/min) and maximum K+ conductance (mM/min/mV) were 3.54 +/- 1.65 and 0.036 +/- 0.02 in cetrimide, and 1.85 +/- 0.35 and 0.021 +/- 0.009 in potassium bromate, respectively. In view of these findings, the influence of the active transport mechanism to K+ concentrations are discussed in comparison with dynamic changes in endolymph K+ induced by asphyxia and ethacrynic acid.

Animals↗
PubMed1977

The effect of oral potassium supplements on plasma potassium in normokalaemic and hypokalaemic patients.

Thirteen out of 44 patients taking bendrofluazide 10 mg daily became hypokalaemic over a period of three months. Oral potassium supplements of 3.6 grams daily (48 mmol) given in addition to bendrofluazide for a further period of 3 months raised plasma potassium level significantly in hypokalaemic patients only. We conclude that where patients on diuretic therapy are followed up with plasma potassium measurements, it is generally necessary to prescribe oral potassium in the presence of hypokalaemia only.

Administration, Oral↗
PubMed1982

Theoretical effect in human heart disease of low-sodium high-potassium diet therapy on intracellular adsorbed sodium and potassium.

Clinical study has shown that high-potassium in addition to low-sodium diet therapy for human cardiac disease is much more effective than low-sodium diet alone or than the usual drug therapies. Analyzed by the association-induction concept of adsorbed cellular sodium and potassium, the clinically measured changes of blood sodium and potassium due to the combined diet would be expected to yield marked improvement in intracellular sodium and potassium because of the nonlinear shape of the expected cation adsorption curves. Indicated is a significant approach toward restoring normality of the intracellular cationic environment in cardiac patients.

Adsorption↗
PubMed2004

Role of potassium channels, the sodium-potassium pump and the cytoskeleton in the control of dog sperm volume.

Response to osmotic shock is an important aspect of mammalian sperm physiology. In this study we recorded volume changes of dog spermatozoa at 39, 33, and 25 degrees C under isotonic conditions and following hypotonic shock. Cell volume measurements were performed electronically in saline solutions of 300 and 150 mOsmol kg(-1), and Percoll-washed preparations were compared with unwashed samples. The involvement of potassium channels in volume control was tested by treatment with quinine, while the involvement of the plasma membrane Na(+)-K+ pump was tested by treatment with ouabain. The role of the cytoskeleton was investigated by treatment with colchicine and cytochalasin D. The number of cell populations observed varied with temperature and tonicity. In both types of sperm preparations, between two and three populations were present under isotonic conditions at 25 degrees C whereas at 39 and 33 degrees C only one population was detected. Hypotonic stress at the higher temperatures caused the single population to swell, whereas at 25 degrees C it resulted in a population of cells whose modal volume was similar to that of the middle isotonic sub-population. Both quinine and the cytoskeletal inhibitors markedly increased swelling both under hypotonic conditions at 39 degrees C and under isotonic conditions at 25 degrees C. However, little or no effect of ouabain was observed. We conclude that in dog spermatozoa swelling in response to hypotonic conditions is minimised through the activity of potassium channels and the presence of an intact cytoskeletal network. Under isotonic conditions at 25 degrees C, a considerable proportion of the sperm population is already swollen; this swelling varies between individual males and appears to be due to lowered cytoskeletal and potassium channel activity.

Animals↗
PubMed1993

Structure of a citrate double salt: potassium dihydrogen citrate-lithium potassium hydrogen citrate monohydrate.

The crystal structure of a double salt of potassium dihydrogen citrate and lithium potassium hydrogen citrate monohydrate has been determined. One potassium ion is coordinated with eight O atoms and the other with nine O atoms at M--O distances in the range 2.660 (1) to 3.139 (1) A. Two of these O atoms are shared by both potassium ions. The lithium ion is tetrahedrally surrounded by four O atoms at distances in the range 1.870 (3) to 1.988 (3) A. This crystal structure contains nine hydrogen bonds in the asymmetric unit. The water molecule connects different citrate ions along the c direction by hydrogen bonding.

Citrates↗
PubMed1999

Voltage-gated, margatoxin-sensitive potassium channels, but not calcium-gated, iberiotoxin-sensitive potassium channels modulate acetylcholine release in rat striatal slices.

We evaluated the effects of iberiotoxin, an inhibitor of Slo-type Ca2+-activated potassium channels and two inhibitors of Shaker-type voltage-gated potassium channels margatoxin and dendrotoxin on acetylcholine outflow in rat striatal slices. An in vitro perfusion with 100 nM margatoxin or dendrotoxin induced a concentration-dependent and tetrodotoxin-sensitive enhancement in spontaneous acetylcholine release. In contrast, a perfusion with iberiotoxin did neither modulate basal, nor electrically- or N-methyl-d-aspartate-induced transmitter release. Therefore, Slo-type Ca2+-activated K+-channels do not seem to contribute significantly to cholinergic neurotransmission within rat striatal slices. As the Kv1.2 subtype represents the only common high affinity binding site of margatoxin and dendrotoxin and the effects of these toxins are not additive, this subtype is suggested to be the channel utilized by margatoxin and dendrotoxin to release acetylcholine in this model.

Acetylcholine↗
PubMed1991

Potassium substitution via the oral route: does its efficacy depend on the anion of the potassium salt?

In an open, randomized study, we investigated the effect of oral potassium chloride (KCl) and of potassium citrate/bicarbonate (K-cit/bic) in 42 patients with hypokalemia (less than or equal to 3.5 mmol/l). In both groups 80 mmol K+ were administered daily. The parameters examined were serum potassium concentration, acid-base status, and urinary electrolyte excretion. Parameters were evaluated on days 0, 2, 4, and 6. With KCl, [K+] increased from 3.2 +/- 0.2 (mean +/- SD) on day 0 to 3.8 +/- 0.4 mmol/l on day 2 (p less than 0.005) and 4.0 +/- 0.5 mmol/l on day 4 (p less than 0.005). On day 6 [K+] was also 4.0 +/- 0.4 mmol/l (p less than 0.005 vs day 0). With K-cit/bic, [K+] increased from 3.2 +/- 0.2 to 3.7 +/- 0.4 on day 2, 3.9 +/- 0.5 on day 4, and 4.1 +/- 0.6 mmol/l on day 6 (all p less than 0.005 vs day 0). The increase of [K+] was not different between the two groups. Blood pH on day 0 was in the normal range in both groups and did not change significantly during the study. There was a decrease of carbon dioxide partial pressure (pCO2) with KCl from 38.7 +/- 4.9 on day 0 to 36.4 +/- 3.6 on day 2 (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Acid-Base Equilibrium↗
PubMed2004

Streptomyces lividans potassium channel KcsA is regulated by the potassium electrochemical gradient.

It is currently held that the Streptomyces lividans potassium channel, KcsA, requires an intracellular pH<5 to exhibit activity in planar lipid bilayers. Here, we show that KcsA functions well at normal physiological pH in the presence of a potassium electrochemical gradient. Single-channel conductance and open probability increased directly as the extracellular potassium concentration was decreased. Channel activity was sensitive to both the membrane potential and the size of the gradient, thus indicating that gating of the channel depends on both components of the electrochemical potential. When [K(+)(in)]/[K(+)(ex)] was 200 mM/10 mM, chord conductance was 24pS with subconductance 15pS; open probability was 0.9. The permeability series was K(+) > Rb(+) >>> Cs(+); K(+) selectivity over Rb(+) was 1.2-fold and selectivity over Na(+) was 12-fold. The channels were disrupted by intracellular Na(+) and blocked by intracellular Ba(2+). A hypothetical supramolecular model for the channel is presented.

Bacterial Proteins↗
PubMed2003

Increased dietary potassium and magnesium attenuate experimental volume dependent hypertension possibly through endogenous sodium-potassium pump inhibitor.

We and others have shown that inhibition of cardiovascular muscle (CVM) cell Na+,K-ATPase activity (NKPTA) due to increased level of endogenous sodium potassium pump inhibitor (SPI) is involved in the mechanism of volume expanded (VE) experimental and human essential hypertension (HT). Since diets fortified with very high potassium (K) or very high magnesium (Mg) decrease blood pressure (BP), we have examined the effect of a moderate increase in dietary K alone and a moderate increase in dietary K and Mg on plasma levels of SPI, CVM cell NKPTA, and BP in reduced renal mass (RRM)-salt HT rats, a classical model of VE HT. Seventy Percent-RRM rats were divided in four dietary groups, (1) Na free and normal K and Mg (0Na-K-Mg); (2) normal Na, K and Mg (Na-K-Mg); (3) normal Na and high K (2 x normal), and normal Mg (Na-2K-Mg); and (4) normal Na and high K (2 x normal), and high Mg (2 x normal) (Na-2K-2Mg). As expected, compared to control 0Na-K-Mg rats, Na-K-Mg rats developed HT. Blood pressure increased significantly less in Na-2K-Mg rats whereas, BP did not increase in Na-2K-2Mg rats. Hypertension in NA-K-Mg rats was associated with an increase in plasma SPI and digitalis like factor (DIF) and a decrease in renal and myocardial NKPTA. However, doubling the Mg along with K in the diet (Na-2K-2Mg) normalized SPI and DIF and increased myocardial and renal NKPTA, compared to control 0Na-K-Mg rats. Also, compared to 0Na-K-Mg rats, water consumption, urine excretion, urinary sodium excretion urinary potassium excretion (U(Na)V), and (U(K)V) increased in the other three groups, more so in Na-2K-2Mg rats. These data show that K and Mg have additive effects in preventing an increase in SPI, thus probably preventing the BP increase in RRM rats.

Animals↗
PubMed1979

The effect on plasma potassium of a combined preparation of frusemide and slow-release potassium chloride (Diumide-K Continus tablets).

An open trial was carried out on ten middle-aged and elderly patients in cardiac failure to assess the effect on plasma potassium levels of one or more tablets containing 40 mg frusemide and a controlled-release formulation containing 600 mg potassium chloride. Patients had previously been maintained on frusemide and potassium supplements given as separate tablets. No significant rise or fall was observed when treatment was changed to the combined tablet.

Administration, Oral↗
PubMed1986

High chronic ambient temperature stress effects on broiler acid-base balance and their response to supplemental ammonium chloride, potassium chloride, and potassium carbonate.

Four experiments were conducted to evaluate the effect of heat stress on acid-base status and the birds' response to supplemental KCl and KCO3. The corn-soybean meal fish-meal basal ration (.73% K+) contained more K+ and Cl- than is recommended by the National Academy of Sciences for chicks reared under near optimal conditions (24 C and 55% relative humidity). Chicks reared under continuous thermostress (35 C, 70% relative humidity) exhibited panting phase blood alkalosis (pH of 7.46). Supplementing drinking water with .2% NH4Cl reduced panting phase blood pH to normal values and increased live weight gain (23%) and feed efficiency (7.7%). Supplementing drinking water with .15% KCl also increased (P less than .05) live weight gain (46%) and feed efficiency (15.4%) but did not affect (P less than .46) blood pH. A significant (P less than .01) interaction existed between NH4Cl and KCl for body weight gain. Adding .2% NH4Cl to broiler drinking water reduced the level of KCl required in drinking water to optimize weight gain to .1% KCl. Potassium chloride alone, or with NH4Cl, can alleviate some consequences of heat stress, but supplementing drinking water with a high level of NH4Cl (.5%) decreased (P less than .05) blood pH to acidotic levels and reduced body weight gain. Potassium chloride supplementation exacerbated NH4Cl toxicity. Potassium carbonate reduced (P less than .05) body weight gain indicating that the response may not be attributed to K+ alone. Beneficial effects of NH4Cl therapy for heat stressed broilers are speculative.

Acid-Base Equilibrium↗
PubMed2004

Comparative study of the efficacy of potassium magnesium L-, D- and DL-aspartate stereoisomers in overcoming digoxin- and furosemide-induced potassium and magnesium depletions.

Potassium and magnesium aspartate (K,Mg aspartate) is used in treating and preventing cardiac disruptions caused by electrolytic disturbances, primarily low potassium (K) and magnesium (Mg) levels (e.g. in the treatment with cardiac glycosides and diuretic drugs). Widely used, K,Mg aspartate is synthesized from aspartic acid representing a racemic mix of L- and D-stereoisomers. Differences in metabolism and utilisation of D- and L-amino acids probably have an effect on the pharmacological properties of K,Mg L- and D-aspartates, and what is more, pharmacological doses of magnesium and potassium salts may induce toxicity, which differs according to the nature of the anions. Therefore, the purpose of the present work was to study the effect of intravenously administered K,Mg L-aspartate in comparison with its D- and DL-stereoisomers on K and Mg restoration rates in plasma, erythrocytes and myocardium and to evaluate the urine excretion rate of amine nitrogen and Mg in digoxin and furosemide treated rats. To induce Mg depletion, male rats, weighing 180-200 g, were given furosemide and digoxin at doses of 30 mg/kg (i.p.) and 0.25 mg/kg (i.p.) daily for 14 days. After 14 days K,Mg L-, D- and DL-aspartates were administered with simultaneous furosemide and digoxin treating at dose of 100 mg/kg (i.v.), which corresponds to 46.95 mg of Mg aspartate (i.e. Mg = 3.96 mg) and 53.05 mg of K aspartate (i.e. K = 12.12 mg) per kg bodyweight. Erythrocyte, plasma and urine Mg levels were measured by colorimetric assay using the method based on the staining reaction of Mg and thiazole yellow. Myocardium Mg and K content and erythrocyte K levels were determined by flame atomic absorption spectroscopy. The level of amine nitrogen was measured by colorimetric assay using the method based on the staining reaction with ninhydrin. It was shown that K,Mg L-aspartate administration leads to higher compensation of K and Mg deficiency in rats with furosemide and digoxin induced K and Mg depletion, as compared with D- and DL-stereoisomers. According to the K and Mg deficiency correction rate, K,Mg aspartates may be ranged in the following order: K, Mg L-aspartate > K,Mg DL-aspartate > K,Mg D-aspartate. It was shown that after administration of K,Mg L-aspartate, daily urine excretion of amine nitrogen and Mg is less than after D- and DL-stereoisomer administration. According to the quantity of excreted amine nitrogen and Mg in urine, K,Mg aspartates may be ranged in the following order: K,Mg D-aspartate = K, Mg DL-aspartate > K,Mg L-aspartate. So, K,Mg L-aspartate is more beneficial in the treatment of several forms of primary Mg and K deficiency than K,Mg DL-aspartate and K, Mg D-aspartate.

Amines↗
PubMed1982

The effect of potassium canrenoate (Aldactone) on the norepinephrine metabolism and potassium ionic currents of the heart.

Under experimental conditions, potassium canrenoate causes a significant increase in [3H]norepinephrine (NE) uptake by the heart, although the NE content remains unchanged. The increased NE uptake and unchanged NE content indicate an augmented NE turnover caused by the drug. In saluretic-pretreated animals, the intracellular hypopotassemia can be restored by Aldactone. This effect can be explained by the inhibition of the outward potassium current. When we simulated the pathophysiological conditions of the acute phase of myocardial infarction by using a K+-rich superfusate to partially depolarize the myocardial cells, slow action potentials were elicited by NE in isolated papillary muscles. Our microelectrode experiments revealed that Aldactone, by its blocking effect on the potassium conductance, increases the duration of the slow action potentials and decreases the threshold NE concentration required to elicit the slow responses. However, in clinical conditions with a higher level of circulating catecholamine and/or hyperpotassemia, the administration of the drug has a considerable risk of provoking arrhythmias.

Animals↗