Active sodium and potassium transport in high potassium and low potassium sheep red cells

The kinetic characteristics of the ouabain-sensitive (Na + K) transport system (pump) of high potassium (HK) and low potassium (LK) sheep red cells have been investigated. In sodium medium, the curve relating pump rate to external K is sigmoid with half maximal stimulation (K_1/2) occurring at 3 mM for both cell types, the maximum pump rate in HK cells being about four times that in LK cells. In sodium-free media, both HK and LK pumps are adequately described by the Michaelis-Menten equation, but the K_1/2 for HK cells is 0.6 ± 0.1 mM K, while that for LK is 0.2 ± 0.05 mM K. When the internal Na and K content of the cells was varied by the PCMBS method, it was found that the pump rate of HK cells showed a gradual increase from zero at very low internal Na to a maximum when internal K was reduced to nearly zero (100% Na). In LK cells, on the other hand, no pump activity was detected if Na constituted less than 70% of the total (Na + K) in the cell. Increasing Na from 70 to nearly 100% of the internal cation composition, however, resulted in an exponential increase in pump rate in these cells to about ⅙ the maximum rate observed in HK cells. While changes in internal composition altered the pump rate at saturating concentrations of external K, it had no effect on the apparent affinity of the pumps for external K. These results lead us to conclude that the individual pump sites in the HK and LK sheep red cell membranes must be different. Moreover, we believe that these data contribute significantly to defining the types of mechanism which can account for the kinetic characteristics of (Na + K) transport in sheep red cells and perhaps in other systems.     

Brain tissue potassium in normal and potassium depleted rats

The potassium concentration of muscle, brainstem and diencephalon were studied in normal and potassium-depleted rats. With 13% depletion of muscle potassium there was a 2.1% and 2.8% decrease in brainstem and diencephalon tissue potassium respectively. With 34% depletion of muscle potassium there was a 1.9% and 4.0% decrease in brainstem and diencephalon tissue potassium. These small decreases in regional brain tissue potassium could be related to observed functional alterations in the potassium depleted rat, i.e., altered cerebrospinal fluid bicarbonate regulation and altered control of the pattern of breathing and of body temperature regulation.     

Basolateral K-Cl cotransporter regulates colonic potassium absorption in potassium depletion

Active potassium absorption in the rat distal colon is electroneutral, Na(+)-independent, partially chloride-dependent, and energized by an apical membrane H,K-ATPase. Both dietary sodium and dietary potassium depletion substantially increase active potassium absorption. We have recently reported that sodium depletion up-regulates H,K-ATPase alpha-subunit mRNA and protein expression, whereas potassium depletion up-regulates H,K-ATPase beta-subunit mRNA and protein expression. Because overall potassium absorption is non-conductive, K-Cl cotransport (KCC) at the basolateral membrane may also be involved in potassium absorption. Although KCC1 has not been cloned from the colon, we established, in Northern blot analysis with mRNA from the rat distal colon using rabbit kidney KCC1 cDNA as a probe, the presence of an expected size mRNA in the rat colon. This KCC1 mRNA is substantially increased by potassium depletion but only minimally by sodium depletion. KCC1-specific antibody identified a 155-kDa protein in rat colonic basolateral membrane. Potassium depletion but not sodium depletion resulted in an increase in KCC1 protein expression in basolateral membrane. The increase of colonic KCC1 mRNA abundance and KCC1 protein expression in potassium depletion of the rat colonic basolateral membrane suggests that K-Cl cotransporter: 1) is involved in transepithelial potassium absorption and 2) regulates the increase in potassium absorption induced by dietary potassium depletion. We conclude that active potassium absorption in the rat distal colon involves the coordinated regulation of both apical membrane H,K-ATPase and basolateral membrane KCC1 protein.     

Clinical potassium problems

Alterations in serum potassium are common in many diseases. In a series of 390 determinations of serum potassium, the levels found were low in 24 per cent and high in 2.6 per cent. The major causes of low serum potassium are (1) decreased potassium intake due to intravenous feedings which do not contain potassium; (2) increased loss of potassium in the urine due to accelerated tissue breakdown, or renal lesions; (3) loss from the gastrointestinal tract due to diarrhea, or fistulae, and (4) shift between serum and cells, due to metabolic causes, drugs or changes in pH. The major cause of high serum potassium is uremia with renal retention.Clinical symptoms and signs of low body potassium include muscle weakness and paralysis, which may lead to death in respiratory failure if not corrected, tachycardia, gallop rhythm, dilatation of the heart. The electrocardiogram shows inverted, low amplitude, or isoelectric T waves and a prolonged QT interval. Potassium chloride orally, subcutaneously or intravenously is recommended for use in the treatment of potassium deficits. It should not be used in the presence of oliguria or anuria or dehydration. The amounts of potassium necessary to correct deficits vary widely and cannot be predicted from the serum level. Special reference is made to the prevention and therapy of potassium deficits in diabetic acidosis. High serum potassium levels are difficult to correct. Suggested measures are administration of glucose, insulin or calcium, gastric or peritoneal lavage or use of the artificial kidney.     

Fixation of proteins by osmium tetroxide potassium dichromate and potassium permanganate

Summary The crosslinking abilities of osmium tetroxide, potassium dichromate and potassium permanganate towards bovine serum albumin and bovine -globulin were investigated by chromatography with Sephadex G-200. Osmium tetroxide had a moderate crosslinking ability towards these proteins, the others had little or none. Chromatography with Sephadex G-50 permitted the oxidative cleavage of the proteins by these oxidative fixation agents to be studied. Potassium permanganate caused much fragmentation of the proteins and destruction of the tyrosine and tryptophan residues. Osmium tetroxide and potassium dichromate caused only a small amount of protein cleavage. These results were corroborated by polyacrylamide gel electrophoresis and viscosimetric studies. The significance of the results for tissue fixation is discussed.     

Plant responses to potassium deficiencies: a role for potassium transport proteins

The availability of potassium to the plant is highly variable, due to complex soil dynamics, which are strongly influenced by root-soil interactions. A low plant potassium status triggers expression of high affinity K+ transporters, up-regulates some K+ channels, and activates signalling cascades, some of which are similar to those involved in wounding and other stress responses. The molecules that signal low K+ status in plants include reactive oxygen species and phytohormones, such as auxin, ethylene and jasmonic acid. Apart from up-regulation of transport proteins and adjustment of metabolic processes, potassium deprivation triggers developmental responses in roots. All these acclimation strategies enable plants to survive and compete for nutrients in a dynamic environment with a variable availability of potassium.     

Extracellular potassium inhibits Kv7.1 potassium channels by stabilizing an inactivated state

Kv7.1 (KCNQ1) channels are regulators of several physiological processes including vasodilatation, repolarization of cardiomyocytes, and control of secretory processes. A number of Kv7.1 pore mutants are sensitive to extracellular potassium. We hypothesized that extracellular potassium also modulates wild-type Kv7.1 channels. The Kv7.1 currents were measured in Xenopus laevis oocytes at different concentrations of extracellular potassium (1–50 mM). As extracellular potassium was elevated, Kv7.1 currents were reduced significantly more than expected from theoretical calculations based on the Goldman-Hodgkin-Katz flux equation. Potassium inhibited the steady-state current with an IC₅₀ of 6.0 ± 0.2 mM. Analysis of tail-currents showed that potassium increased the fraction of channels in the inactivated state. Similarly, the recovery from inactivation was slowed by potassium, suggesting that extracellular potassium stabilizes an inactivated state in Kv7.1 channels. The effect of extracellular potassium was absent in noninactivating Kv7.1/KCNE1 and Kv7.1/KCNE3 channels, further supporting a stabilized inactivated state as the underlying mechanism. Interestingly, coexpression of Kv7.1 with KCNE2 did not attenuate the inhibition by potassium. In a number of other Kv channels, including Kv1.5, Kv4.3, and Kv7.2–5 channels, currents were only minimally reduced by an increase in extracellular potassium as expected. These results show that extracellular potassium modulates Kv7.1 channels and suggests that physiological changes in potassium concentrations may directly control the function of Kv7.1 channels. This may represent a novel regulatory mechanism of excitability and of potassium transport in tissues expressing Kv7.1 channels.     

Removal of potassium chloride by nanofiltration from ion-exchanged solution containing potassium clavulanate

In this study, nanofiltration with NF200 membrane was employed to remove KCl from ion-exchanged solutions containing potassium clavulanate. The pore radius of NF200 membrane was estimated to be around 0.39 nm. The effects of operating pressure on separation performance were investigated in a range of 100–400 psig. The influences of cross-flow velocity (0.14–0.70 cm/s), temperature (4–25 °C), and feed composition were also investigated. In all experiments, clavulanate rejection showed high levels from 0.91 to 0.99, while chloride rejection ranged from 0.06 to 0.54. In a case at an operating pressure of 50 psig and 25 °C, as much as 94% of clavulanate was retained while 94% of chloride was removed, indicating that NF200 membrane was a suitable choice for selectively removing KCl. NF200 membrane also showed a stable performance in the operational stability test with an ion-exchanged solution obtained by treating actual fermentation broth.     

Memory and potassium channels

The K(+)-channels of the surface membrane play a crucial role in the generation of electrical activity of a neuron. There is a large diversity of the K(+)-channels that depends on a great number (over 200) of genes encoding channels proteins. An evolutionary conservation of channel's proteins is determined. The K(+)-channels were found to have a great importance in the memory processes. It was shown on different model systems that K(+)-current of the surface membrane decreases during the learning. The antagonists of K(+)-channels were found to improve the learning and memory. It was revealed in electrophysiological experiments that K(+)-channels antagonists can either themselves induce a long-term synaptic potentiation or intensify the synaptic potentiation induced by a tetanization. The disfunction of K(+)-channels is believed to be an important link in the mechanisms of memory disturbances. In animal mutants with K(+)-channels disfunction, learning and memory are deficient. In behavioral experiments, the use of K(+)-channels openers make the learning worse. Amnesia caused by cerebral ischemia is explained by strong activity of K(+)-channels which not only inhibits neuronal excitement but also causes neurodegeneration. The question on the K(+)-channels involvement into pathophysiology of Alzheimer's disease is discussed. Neurotoxic peptide beta-amyloid, which is supposed to be involved into mechanisms of Alzheimer's disease, modulates K(+)-channels function. The effect of beta-amyloid depends on the subtype of K(+)-channels: A-channels are inhibited, and KDR-channels, on the contrary, become stronger. The effect of the cognitive enhancers (vinpocetine, piracetam, tacrine, linopirdine) on K(+)-current also depends on the subtype of K(+)-channels. Slow-inactivating K(+)-currents (IDR, IK(Ca), IM) are inhibited in the presence of these drugs, while fast-in-activating K(+)-current (A-current) remains unchanged or even increases.     

Trafficking of potassium channels

Recent progress in our understanding of the trafficking of potassium channels can be seen in particular when considering the Kv-type channels. To date, we have discovered that folding of the Kv1.3 T1 domain begins in the ribosomal exit tunnel, and that the cell surface expression of Kv4 channels is enhanced by the presence of two recently identified accessory subunits. Current advances are beginning to enable us to understand the Kv supermolecular complex containing these subunits in crystallographic detail. In addition, determinants that govern the dendritic or axonal targeting of Kv channels have also been identified. In terms of the bigger picture, the careful analysis of gene expression patterns in the brain paves the way for studying trafficking in a physiological context. Indeed, neuronal activity has recently been shown to fine-tune the localization of Kv2.1 channels in microdomains of the neuronal plasma membrane.     

Studies in soil potassium

Summary The Quantity-Intensity relations of labile K in soil relate the intensity (or availability) of labile K to the amount of labile K present. Several soils have been depleted of K by crops, and enriched or depleted of K by other means. Theforms of the Q/I relations for labile K in these soils are almost unaffected by K-depletion, by the fixation of added K on storage, or by the release or fixation of K by heating. The addition of very large amounts of K may cause transient changes, but these changes disappear on storing the soil.So under field conditions depletion of K or Ca + Mg by crops, and the addition of K in fertilisers, are unlikely to alter the form of the Q/I relations of labile K.The release of fixed K from depleted soils was very slow unless the depleted soils were heated. Fixation of added K was more rapid.     

植物钾营养性状的遗传潜力v

钾是植物生长发育所必需的大量元素,是与氮、磷并列的植物营养的“三大要素”之一。不同植物种类或同种类植物的不同品种之间钾营养效率的差异非常显著,这为植物钾营养性状的遗传改良提供了科学依据