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Effect of potassium adaptation on the distribution of potassium, sodium and chloride across the apical membrane of renal tubular cells.

To assess the effect of K adaptation on the electrolyte concentrations of renal tubular cells and on the concentration gradients across the luminal membrane, electron microprobe analysis was employed on freeze-dried cryosections of the renal cortex and on freeze-dried samples of tubular fluid in control and high-K rats. The measurements were performed in individual cells of the proximal and superficial distal tubule and on samples of tubular fluid obtained by free flow micropuncture from proximal and early and late distal collection sites. The ingestion of a potassium-rich diet for at least 10 days together with an acute potassium load of 0.4 mmol/kg/h led to a small increase in potassium concentration of about 7 mmol/kg wet weight (w.w.) in all cell types analysed. In distal convoluted tubule, connecting tubule and principal cells sodium concentration was markedly decreased by 4, 4, and 6 mmol/kg w.w., respectively, while no significant changes in sodium concentration were found in proximal tubule and intercalated cells. No consistent changes in cell chloride could be observed under K adaptation. Analysis of the tubular fluid samples showed that the K concentration gradient across the apical cell membrane of all distal tubular cell types investigated was diminished in the high-K rats. The concentration gradient for sodium entry, however, was clearly enhanced in the distal convoluted tubule, connecting tubule and principal cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Effect of external potassium on the coupled sodium: potassium transport ratio of axons.

1. Resting membrane potential and the current-voltage relation were measured in crayfish giant axons bathed in various potassium solutions with and without ouabain. 2. Ouabain caused a depolarization of the membrane at each [K]o used but did not affect membrane resistance. 3. The ouabain-sensitive transport current was least (3 microamperemeter/cm2) in 0 mM [K]o and greatest (7 microamperemeter/cm2) in 16.2 and 21.6 mM [K]o. 4. The assumption was made an some indirect evidence presented that axons equilibrated in various potassium solutions maintain constant internal sodium and potassium concentrations for up to 3 h. 5. On the basis of this assumption, the apparent ratio of coupled Na : K transport was calculated. It was found to be least (-1.3/1) in 0 mM [K]o and to approach infinity in 16.2 and 21.6 mM [K]o. 6. The data indicate that the apparent variability of the Na : K exchange ratio likely represents an intrinsic property of the exchange mechanism and is less likely to be explained by a fixed-ratio coupled Na : K transport operating in parallel with electro-neutral Na : Na or K : K exchange.

Animals↗

Measurement of potassium absorption during hypokinesia in potassium supplemented and unsupplemented healthy subjects.

Measuring potassium (K+) absorption, and K+ levels in plasma, urine and feces during and after hypokinesia (HK) and K+ supplementation, the aim of this study was to determine if prolonged HK could depress K+ deposition significantly more with or without K+ supplementation. Studies were conducted during 30-days pre-HK, 364-days HK and 30-days post-HK. Forty male healthy volunteers 24.2+/-5.5 years of age were chosen as subjects. They were equally divided in four groups: unsupplemented active control subjects (UACS), unsupplemented hypokinetic subjects (UHKS), supplemented active control subjects (SACS), and supplemented hypokinetic subjects (SHKS). Hypokinetic subjects were walking average distances of 0.5+/-0.2 km day(-1). Active control subjects were running average distances of 5.8+/-1.2 km day(-1). Both SHKS and SACS consumed daily 2.17 mEq elemental potassium per kg body weight. Potassium absorption, fecal and urinary K+ excretion, sodium (Na+) loss, plasma K+ and Na+ level and plasma aldosterone (PA) level did not change in SACS and UACS compared with their pre-HK values. During HK, K+ absorption decreased significantly (P < 0.05) with time, and fecal and urinary K+ loss, urinary Na+ loss, plasma K+ and Na+ levels and PA level increased significantly (P < 0.05) with time in SHKS and UHKS compared with their pre-HK values and their respective active controls (SACS and UACS). During initial 15-days of post-HK, K+ absorption increased significantly (P < 0.05), fecal and urinary K+ excretion, urinary Na+ excretion and plasma K+ and Na+ levels and PA level decreased significantly (P < 0.05) in hypokinetic compared with active control subjects; by the 30th day they approached the control levels. During HK and post-HK, K+ absorption, fecal and urinary K+ losses, urinary Na+ excretion, plasma K+ and Na+ levels and PA level, changed significantly (P < 0.05) more in SHKS than UHKS. Decreased K+ losses during post-HK showed K+ depletion during HK. Decreased K+ absorption with K+ depletion during HK showed decreased K+ deposition. The greater K+ changes in SHKS than UHKS, during HK and post-HK, demonstrated that K+ deposition decreased more with than without K+ supplementation. It was concluded that dissociation between K+ absorption and K+ depletion showed decreased K+ deposition as the main mechanism for K+ depletion during HK.

Absorption↗

Intracellular potassium activity, potassium equilibrium potential and membrane potential of carotid body glomus cells.

The intracellular potassium activity (ai(K)) of glomus cells in isolated rabbit carotid bodies was measured with potassium ion selective microelectrodes (K+ electrodes). The measurements yielded a mean ai(K) value of 33.0 mM in Hepes-buffered Tyrode's solution equilibrated with 100% O2. This value is significantly higher than that predicted by assuming that K+ ions are passively distributed across the membrane of glomus cells. The relationship between the membrane potential (EM) and the equilibrium potential of K+ ions (EK) at various extracellular potassium activities (ao(K] suggests that K+ ions are not involved in the maintenance of the carotid body glomus cell EM.

Animals↗

The effect of AL0671, a novel potassium channel opener, on potassium current in rat aortic smooth muscle cells.

1. We evaluated the mechanism of activation by AL0671, a novel potassium channel opener, of potassium current in rat aortic smooth muscle cells. 2. Under conditions of whole cell recording, AL0671 (1-1000 microM) markedly increased potassium current with a Hill coefficient of 2 and dissociation constant of 1.5 x 10(-4) M. This activation was completely inhibited by intracellular ATP. 3. Under inside-out patch conditions, the ATP-sensitive K+ channels (KATP) treated with AL0671 (100 microM) showed prolongation of the slower open time component and shortening of the slower closed time component without modification of channel conductance.

Animals↗

Effects of aluminum chloride on sodium current, transient outward potassium current and delayed rectifier potassium current in acutely isolated rat hippocampal CA1 neurons.

The effects of aluminum chloride (AlCl3) on sodium current (INa), the transient outward potassium (IA) and delayed rectifier potassium currents (IK) in hippocampal CA1 neurons of rats were studied using the whole cell patch-clamp technique. AlCl3 decreased INa, IA, and IK in a partly reversible, dose and voltage-dependent manner. AlCl3 prolonged the time to peak of INa, and increased the inactivation time constants of INa and IA . In addition, 1000 microM AlCl3 shifted the voltage dependence of steady-state activation of INa, IA and IK toward positive potential, and the voltage dependence of steady-state inactivation of INa, IA toward negative potential. These results imply that AlCl3 could affect the activation and inactivation courses of sodium current and potassium current of rat hippocampal CA1 neurons, which may contribute to damage of the central nervous system by aluminum.

Aluminum Chloride↗

Plasmolemmal potassium gradient does not affect lung protection by an ATP-regulated potassium channel opener.

BACKGROUND: We have previously shown that metabolic arrest induced with ATP-regulated potassium channel openers (PCOs) can improve lung preservation by adding Aprikalim (a PCO, Rhone-Poulene Roher) to modified Euro-Collins solution for pulmonary artery flush. Because the membrane hyperpolarizing effects of a PCO potentially competes with the depolarizing effects of a hyperkalemic solution, this study evaluated the effects of the potassium gradient on PCO-mediated lung protection. STUDY DESIGN: Twenty rabbits underwent lung protection in four groups. Group 1 underwent harvest and reperfusion as a "no ischemia" control. Groups 2, 3, and 4 underwent harvest followed by 18 hours of cold ischemic storage before reperfusion. Groups 1 and 4 received Euro Collins as the pulmonary flush at induction of ischemia. Group 2 received Euro Collins plus Aprikalim (100 microM); and group 3 received lactated Ringer's plus Aprikalim. After ischemic storage, the lungs were reperfused with autologous blood for 2 hours. Every 30 minutes, the lungs were given a 10-minute 100% fractional inspired oxygen (F(i)O(2)) challenge to measure maximal gas exchange as an indication of graft function. RESULTS: Repeated measures ANOVA showed Aprikalim improved graft function after 18 hours of cold ischemia (p < 0.0001). No significant differences were found when Aprikalim was used in either Euro-Collins (group 2) or lactated Ringer's (group 3) solution. CONCLUSIONS: The ability of the PCO Aprikalim to preserve gas exchange in a model of hypothermic pulmonary ischemia-reperfusion injury was not affected by the plasmolemmal potassium gradient. This is consistent with recent findings in myocardial protection studies that the protective effects of PCOs may be intracellular.

Adenosine Triphosphate↗

Potassium ion accumulation slows the closing rate of potassium channels in squid axons.

Potassium ion accumulation in the periaxonal space between squid axonal membrane and the Schwann cell surrounding the axon slows the rate of potassium channel closing to a degree that is consistent with the effect on channel closing of an equivalent change in the bulk external potassium concentration. The alteration of channel gating is independent of membrane potential, V, for V less than or equal to -60 mV, which suggests that the effect is mediated at a site on the outer surface of the membrane, rather than a site within the channel.

Animals↗

Skeletal muscle magnesium and potassium determinations: correlation with lymphocyte contents of magnesium and potassium.

Following a lymphocyte separation technique, the lymphocyte content of magnesium and potassium was determined by atomic absorption spectroscopy in 28 subjects. Simultaneously, skeletal muscle biopsies were obtained by a percutaneous technique and analyzed for magnesium and potassium. In this study there was not significant correlation between the lymphocyte and the skeletal muscle content of magnesium or potassium, except in the group of three normal volunteers and nine patients with mild arterial hypertension.

Aged↗

Ion metabolism in a potassium accumulation mutant of Escherichia coli B. I. Potassium metabolism.

A potassium transport mutant of Escherichia coli is described which is deficient in the intake of potassium. The phenotype of this mutant is characterized by (i) failure to grow in K(+)-deficient medium, (ii) failure to accumulate K(+) in K(+)-deficient medium, (iii) a steady-state intracellular K(+) that varies sigmoidally with the medium K(+) concentration, (iv) a signoidally shaped rate-concentration curve and a curved reciprocal plot for net K(+) uptake kinetics, and (v) a low steady-state flux of potassium associated with a reduced influx rate constant. The data are discussed in terms of the present day models of cation transport. These models have led to four possible explanations of the mutant's phenotype: (i) a selectivity reversal such that intracellular cation binding sites bind another cation instead of K(+); (ii) a structural alteration of cation binding cell proteins so that K(+) is bound by "cooperative binding" (sigmoid isotherm) instead of by simple adsorption (hyperbolic isotherm); (iii) conversion of an enzyme in intermediate metabolism that rate-limits K(+) uptake to an allosteric protein; (iv) conversion of the "carrier protein" for K(+) to an allosteric protein.

Escherichia coli↗

Solubilization of potassium-bearing minerals by a wild-type strain of Bacillus edaphicus and its mutants and increased potassium uptake by wheat.

Two potassium (K)-bearing minerals, Nanjing feldspar and Suzhou illite, were used to investigate K mobilization by the wild-type strain NBT of Bacillus edaphicus, also labeled MPs+, selected for high activity in mobilizing potassium from minerals, and by four of its UV + LiCl mutants, MPs++, MPs+1, MPs+2, and MPs-. In liquid cultures, the five bacterial strains showed better growth on Suzhou illite than on Nanjing feldspar. Suzhou illite was the better potassium source for the growth of the wild type and the MPs++, MPs+1, and MPs+2 mutants. Solubilization of K from its sources by the wild-type NBT and the MPs++ mutant resulted mostly from the action of organic acids and capsular polysaccharides. Oxalic acid seemed to be a more active agent for the solubilization of Nanjing feldspar. Oxalic and tartaric acids were likely involved in the solubilization of Suzhou illite. The MPs- mutant did not produce any organic acid or capsular polysaccharide when grown on the above two K sources. In a pot experiment, wheat (Triticum aestivum L.) 'Yangmai-158' was grown in a yellow-brown soil that had low available K. After inoculation with bacterial strains, B. edaphicus NBT and its four mutants, MPs++, MPs+1, MPs+2, and MPs- (in separate tests), the root growth and shoot growth of wheat were significantly increased by B. edaphicus NBT and the mutants MPs++ and MPs+1. Bacterial inoculation also resulted in significantly higher N, P, and K contents of plant components. The bacteria were able to survive in the wheat rhizosphere soils after root inoculation.

Bacillus↗

The use of the potassium channel activator riluzole to test whether potassium channels mediate the capacity of isoflurane to produce immobility.

UNLABELLED: Inhaled anesthetics produce immobility during noxious stimulation, primarily by actions on the spinal cord. In this study, we examined whether activation of potassium channels of the KCNK subfamily alters volatile anesthetic potency. We measured the change in isoflurane minimum alveolar anesthetic concentration (MAC) during 4-h intrathecal or IV infusions of the nonspecific KCNK activator riluzole in 54 Sprague-Dawley rats. IV or intrathecal infusions of riluzole doses that did not result in permanent injury or death equally decreased isoflurane MAC. We conclude that although riluzole exhibited anesthetic effects, the similar dose response from IV or intrathecal infusion suggests systemic absorption and actions in the brain rather than the spinal cord. IMPLICATIONS: Riluzole, a drug that activates potassium channels and decreases glutamatergic neurotransmission, primarily acts on supraspinal sites to produce immobility in response to noxious stimuli. This finding does not support the hypothesis that potassium channels mediate the capacity of inhaled anesthetics to produce immobility in the face of noxious stimulation.

Anesthetics, Inhalation↗

Ktr-mediated potassium transport, a major pathway for potassium uptake, is coupled to a proton gradient across the membrane in Synechocystis sp. PCC 6803.

Synechocystis sp. PCC 6803 contains a Ktr system and a putative ATP-dependent Kdp system for potassium uptake. We report here that the Kdp system plays only a minor role in potassium uptake under salt and non-stress conditions, unlike the role it plays in Escherichia coli. In Synechocystis, Ktr-mediated potassium transport is dependent on the proton gradient across the membrane.

Bacterial Proteins↗

The responses of chicks to ammonium, calcium, magnesium, potassium and sodium sulphates and to ammonium and potassium carbonates.

The responses of chicks of 14 days of age to increasing levels of dietary anions and cations were investigated in two experiments. Major reductions in weight gains per chick and in gain:feed ratios were observed in chicks as levels of dietary sulphate, with ammonium or potassium cations, were increased from 0 through 5 g. per 100 g. diet. Sodium sulphate had a similar but smaller effect. Calcium and magnesium sulphates increased weight gains and gain:feed ratios at low levels of dietary inclusion. The relative effect of anion and cation were studied in the second experiment. Potassium carbonate reduced weight gains and gain:feed ratio to a greater degree than potassium sulphate; however the higher dietary levels of ammonium carbonate had little effect on chick growth responses in contrast to the major reductions obtained in response to ammonium sulphate. There were no differences between responses of strains of chicks within experiments. None of the salts were lethal at the levels fed.

Ammonium Sulfate↗

Potassium channels and human corporeal smooth muscle cell tone: diabetes and relaxation of human corpus cavernosum smooth muscle by adenosine triphosphate sensitive potassium channel openers.

PURPOSE: Sustained contraction of human corporeal smooth muscle depends on continuous transmembrane calcium flux through voltage gated calcium channels. K channels modulate corporeal smooth muscle membrane potential and, thus, ultimately affect transmembrane calcium flux. Therefore, we characterized relaxation responses elicited by the K channel modulators pinacidil and levcromakalim on isolated human corporeal tissue strips. We also evaluated the possibility that there may be alterations in adenosine triphosphate sensitive K channel pharmacology/function related to the presence of diabetes mellitus. MATERIALS AND METHODS: A total of 215 isolated human corporeal tissue strips obtained from 57 male patients with organic erectile dysfunction were investigated. Cumulative concentration-response curves were constructed at half log increments for steady state relaxation responses elicited by pinacidil and levcromakalim on equivalently phenylephrine pre-contracted (to approximately 75% of maximum) isolated corporeal tissue strips. Potassium currents were measured using the cell attached whole cell patch clamp technique on freshly isolated corporeal smooth muscle cells. RESULTS: A concentration dependent, glibenclamide sensitive relaxation response of phenylephrine pre-contracted corporeal tissue strips was observed for pinacidil and levcromakalim. Consistent with such observations, electrophysiological recordings on freshly isolated myocytes revealed that pinacidil (10 microM.) and levcromakalim (10 microM.) induced whole cell potassium currents that were blocked by glibenclamide (10 microM.). In addition, statistical analysis revealed that phenylephrine pre-contracted corporeal tissue strips from patients without diabetes were more sensitive to relaxation by both compounds than corporeal tissue strips excised from those with diabetes. Furthermore, relaxation responses elicited by pinacidil and levcromakalim were not affected by charybdotoxin or 4-aminopyridine but were completely reversed by KCl or tetraethylammonium chloride. CONCLUSIONS: These data indicate that the adenosine triphosphate sensitive K channel subtype is likely to have an important role in the relaxation of isolated corporeal tissue strips and, moreover, they are the molecular target for the K channel modulators/openers levcromakalim and pinacidil. Such observations are consistent with the supposition that alterations in the structure/function/activity of these potassium channels may underlie at least some aspects of observed diabetes related differences in tissue sensitivity to K channel modulators.

Adenosine Triphosphate↗

The effects of level of expression of a jellyfish Shaker potassium channel: a positive potassium feedback mechanism.

1. When jellyfish Shaker potassium channels (jShak2) are heterologously expressed in Xenopus oocytes at different levels they demonstrate density-dependent changes in electrical and kinetic properties of macroscopic currents. 2. The activation and inactivation properties of jShak2 channels depend on the extracellular potassium concentration. In this study we present experimental data which show that expression-dependent changes in kinetic and electrical properties of jShak2 macroscopic currents can be explained by the positive feedback effect of dynamic accumulation of K+ in the perimembranal space.

Animals↗

Sensitivity of the slow component of the delayed rectifier potassium current (IKs) to potassium channel blockers: implications for clinical reverse use-dependent effects.

The slow delayed rectifier potassium current (I(Ks)) is unique in its slow activation and deactivation kinetics. It is important during cardiac repolarization, especially when the heart rate is fast. We compared the effects of quinidine, procainamide, sotalol, and amiodarone on I(Ks) and correlated the findings with the clinical reverse use-dependent effects of potassium channel blockers. Human minK RNA was obtained by reverse transcription-polymerase chain reaction using explanted human heart. The RNA was injected into Xenopus oocytes for heterologous expression of I(Ks). A two-electrode voltage clamp technique was performed to investigate the I(Ks). We demonstrated that quinidine, sotalol and procainamide had no effects on I(Ks) up to a concentration of 300 microM while amiodarone inhibited I(Ks) in a concentration-dependent manner starting from 10 microM. The inhibition by amiodarone was state-dependent with gradual unblocking after depolarization. The degree of inhibition was 53% immediately after depolarization and 19% at the end of a 5-second depolarization. I(Ks) is 30 times more sensitive to amiodarone than to quinidine, sotalol, and procainamide. Quinidine, sotalol and procainamide have reverse use-dependent effects while amiodarone does not. This is compatible with the hypothesis that no inhibition of I(Ks) at clinical concentrations contributes to the clinical reverse use-dependent effects.

Amiodarone↗

Potassium perchlorate, potassium iodide, and propylthiouracil: promoting effect on the development of thyroid tumors in rats treated with N-bis(2-hydroxypropyl)-nitrosamine.

The effect of 1000 ppm potassium perchlorate (KClO4), 1000 ppm potassium iodide (KI) or 1000 ppm propylthiouracil (PTU) in the diet on the development of thyroid tumors was studied histologically and biochemically in Wistar rats given a single ip injection of 280 mg of N-bis(2-hydroxypropyl)nitrosamine (DHPN) per 100 g body weight. Basal diet containing 100 ppm KClO4, 1000 ppm KI or 1000 ppm PTU was given for 19 weeks from week 2 to week 20. The incidence of thyroid adenomas at the end of week 20 of the experiment was 100% (20/20) in rats treated with DHPN followed by KClO4, 85% (17/20) in rats given DHPN followed by KI, 95% (19/20) in rats given DHPN followed by PTU, and 5% (1/20) in rats given DHPN alone. The incidence of thyroid cancers was 100% (20/20) in rats treated with DHPN followed by KClO4, 65% (13/20) in rats treated with DHPN followed by KI and 0% (0/20) in rats treated with DHPN followed by or not followed by PTU. Rats given KClO4, KI or PTU alone and untreated rats had no thyroid tumors. The mean values of TSH in serum were 2.94 +/- 0.79 ng/ml in rats treated with DHPN followed by KClO4, 9.40 +/- 16.0 ng/ml in rats treated with DHPN followed by KI and 60.94 +/- 20.60 ng/ml in rats treated with DHPN followed by PTU. It was confirmed that (1) KClO4, PTU and KI promote the development of thyroid tumor in rats treated with DHPN, (2) the promoting effect of KClO4 or KI is stronger than that of PTU and (3) the value of TSH in serum is not parallel to the promoting effect on the development of thyroid tumor.

Animals↗