Potassium cellular uptake

In a starved patient, the secretion of insulin is decreased in response to the low carbohydrate intake. Catabolised fats and protein are used for energy. This results in an intracellu+llar loss of electrolytes, in particular phosphates. When the patient starts to feed, a sudden shift from fat to carbohydrate metabolism occurs and secretion of insulin increases. This stimulates cellular uptake of magnesium, phosphate and potassium, which can lead to hypophosphataemia,... 

Hjqiochloremia is common in gastrointestinal disease (Svendsen et al 1979), because of the loss of gastric hydrochloric acid in high volume reflux from the stomach (in proximal enteritis and grass sickness) and the secretion and/or lack of absorption of chloride in severe colitis. It may also occur in exhausted horse syndrome, chronic compensated respiratory acidosis and following furosemide (frusemide) administration. Hypochloremia in the absence of hyponatremia results in a metabolic alkalosis (Corley Marr 1998). The alkalosis associated with hypochloremia may also result in increased cellular uptake of potassium, leading to hypokalemia (Schaer 1999). 

Indomethacin appears to be the NSAID most frequently associated with the development of hyperkalemia, including patients without apparent risk factors [58]. In addition to the known effects of NSAIDs on potassium delivery to the distal tubule and their inhibition of the renin-angiotensin and aldosterone pathways, indomethacin may have a direct effect to limit cellular uptake of potassium [59]. 

The small fraction (2%) of the total body pt)tassium which is in the extracellular compartment is distributed proportionately between the interstitial and plasma spaces. The concentration in serum is around 4.5 mmol/l. Whereas serum potassium concentration does not vary appreciably in response to water loss or retention, factors which cause even a small or sudden shift of intracellular potassium will cause a big change in the ECF potassium content and concentration. Cellular uptake of potassium is stimulated by insulin. Of particular im wrtance is the reciprocal relationship between potassium and hydrogen ions. Many hydrogen ions are buffered inside cells. As the concentration of hydrogen ions increases with the development of acidosis, potassium ions arc displaced from the cell in order to maintain... 

B. Insulin. Blood glucose is lowered directly by the stimulation of cellular uptake and metabolism of glucose. Cellular glucose uptake Is accompanied by an intracellular shift of potassium and magnesium. Insulin also promotes glycogen formation and lipogenesis. 

Potassium concentration in plasma is dependent on renal function and acid-base balance. Mineral-ocorticoids promote the renal excretion of potassium, and insulin favors cellular uptake (Table 5). 

Five pathways for lithium transport in erythrocytes have been described [34] (1) sodium-lithium exchange, (2) anion exchange, (3) leak, (4) sodium-potassium ATPase, and (5) sodium-potassium cotransport. Lithium-sodium countertransport (LSC), anion exchange, and the leak mechanism are thought to be the most important transport routes for lithium in vivo [34]. All are potentially bidirectional, but the overall direction of flow under physiological conditions is efflux from the cell for LSC and cell uptake with the anion exchange mechanism [35]. A proportion of both cellular uptake and efflux of lithium can be attributed to passive diffusion. 

Figure 1. Outflow dilution curves from a blood-perfused isolated dog heart fitted with the axially-distributed capillary-isf model of Bassingthwaighte (1974). Note that the tail of the model potassium curve is too high - the model is inadequate, lacking cellular uptake.

Il.f.l.1. Insulins. Insulin is the most effective of diabetes medications. Insulin has profound effects on carbohydrate, protein, fat metabolism and electrolytes. It has anabolic and anticatabolic actions. In a state of insulin deficiency, glycogenesis, glucose transport, protein synthesis, triglyceride synthesis, LPL activity in adipose tissue, cellular potassium uptake all decrease on the other hand, gluconeogene-sis, glycogenolysis, protein degradation, ketogene-sis, lipolysis increase. 

Membrane proteins carry out a wide range of critical functions in cells, and they include passive and active transporters, ion chamiels, many classes of receptors, cellular toxins, proteins involved in membrane trafficking, and the enzymes that facilitate electron transport and oxidative phosphorylation. For example, the voltage-gated ion channels that facilitate the passive diffusion of sodium and potassium across the axonal membrane are responsible for the formation of an action potential. Active transport proteins establish ion gradients and are necessary for the uptake of nutrients into cells. Soluble hormones bind to membrane receptors, which then regulate the internal biochemistry of the cell. 

The hydrated thallous ion is similar in size to the hydrated potassium ion, and early literature reported that the uptake of T1 cations in muscle cells made use of the specific uptake mechanism developed for potassium. However, later studies, taking account of the complexity of potassium transport, and the different types of potassium channels, have found some differences between the cellular T1 uptake and the potassium uptake. Thus, digoxin that inhibits the Na/K ATP-ase enzyme system as well as the potassium ion-transport, did not affect the ° T1 transport. 

Hyperkalemia P2-Agonists Promote cellular potassium uptake Salbutamol,Terbutaline... 

Proposed mechanism of toxicity is blockage of cellular efflux of potassium, but not uptake, causing hypokalemia, which maybe severe... 

The organic molecules in cells are mainly anionic. Sodium, as Na, cannot be allowed to neutralize these negative charges of the non-metal compounds inside cells because its external concentration (in the sea) is too high (10 m) and its entry would result in too great a cellular osmotic pressure. For this reason, Cl" also had to be largely rejected. Instead, potassium, K+, is selected for the uptake into the cytoplasm. Neither of these cations binds to organic molecules. Calcium, as Ca +, is also deleterious inside cells because at its environmental concentration (10 m) it... 

Osmo- and ion-regulation play a pivotal role in the cellular metabolism of an animal and its imbalance leads to changes in various physiological and biochemical functions (Moorthy et al., 1984). For maintenance of osmo-concentration of body fluids, sodium, potassium and calcium ions are essential and their role in this aspect has been well demonstrated in molluscs (Schoffeniels and Gilles, 1972). The ATPase enzyme complex system helps in the uptake of such vital ions from the external medium into the body fluids. 

MA and mouse cell poly(A)-containing MA translation stimulated EMC viral MA translation. They also measured the cellular Na /K ATPase activity (the enzyme responsible for the maintenance of the monovalent ion gradient) at different times after infection by estimating the uptake into cells of the potassium ion analogue, (42). Uj to 4 hours after infection no difference in the amount of %b" uptake was observed. Yet, cellular protein synthesis inhibition takes place soon after infection.and is nearly complete by 5 hours after infection. The uptake of Rb decreased precipitously after 4 hr, coinciding with the peak of viral protein synthesis. This suggests that either the Rai /K ATPase activity is severly inhibited or that the plasma membrane becomes leaky to monovalent ions. The result of either is the breakdown of the monovalent ion gradient and an increase in the intracellular sodium ion concentration. However, this phenomenon occurs late in infection, several hours after the onset of cellular protein synthesis inhibition. Thus, it cannot explain the early inhibition of cellular protein synthesis. 

The second question concerns the fact that insulin action involves not only effects on glucose uptake, but other effects such as changes in phosphate turnover (Stadie, 1954) and the cellular accumulation of potassium (Verzdr, 1952), as well as effects on protein synthesis (Bouckaert and de Duve, 1947). Are these changes simply the secondary consequence of a primary insulin action upon cell permeability to glucose We do not know. Despite the appeal of a single unitary mechanism for insulin action, the possibility of direct effects of insulin on events other than glucose transfer cannot be ruled out. 

Both sodium and potassium are rather abundant in the Earth s surface (Na, 2.6% K, 2.4%), but potassium, due to its greater solubility and subsequent uptake by plant life, is much less prevalent in the seas. Indeed, potassium is so vital to plants that its major use, usually as the chloride or sulfate, is in fertilizers. This is certainly not a newly recognized technology. Even centuries ago, farmers knew that spreading wood ashes on their lands made crops grow better. We now recognize that the potassium in these ashes was primarily responsible for the effect. Both sodium and potassium ions are present in plants and animals and are essential for normal biochemical functions, particularly for the maintenance of the concentrations of ions across various cellular membranes, enzyme functions, and the firing of nerve impulses. 

Insulin is a powerful positive inotropic drug. It increases the cardiac output and HR due to increased catecholamine discharge and calcium uptake by heart cells. Insulin reduces plasma potassium levels, thereby increasing cellular transmission and automaticity [32]. The first reported case of a pahent with acute propafenone poisoning and treatment with high-dose insulin and glucose ... 

If the fish survives the initial influx of transition metal ions, it may be able to undergo acclimatory responses that will reduce the giU uptake of transition metals. This can occur by decreasing the rates of metal influx into the giU cells. The fish can also alter the production of metallothioneins, thereby tying up the toxic metal ions before they can bind to the transporter proteins. The fish wiU live if the flow of the metal ions can be attenuated enough to allow the sodium-potassium and the calcium-magnesium pumps to continue to function. The fish dies if the metal influx overwhelms the cellular defenses, binds to the pumps, and reduces their performance. 

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