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It has antiporter- like activity, but since it moves both molecules against their concentration gradients it is not a true antiporter, which would require one solute to move with its gradient, not against it. Its simple function is to pump 3 sodium ions out for every 2 potassium ions taken in and since they both have equal ionic charges, this creates a electrochemical gradient between a cell and its exterior. The protein can also let the reverse operation happen, thus harnessing the energy it has stored in the form of an electric field potential. The reverse process is, unlike the forward, spontaneous. Sodium–potassium pumps[edit]The sodium pump is a membrane protein that uses energy in the form of adenosine triphosphate to perform active transport of sodium ions out of the cell in exchange for potassium ions into the cell. For every adenosine triphosphate molecule that the pump uses, three sodium ions are exported, while two potassium are imported; there is hence a net export of a single positive charge per pump cycle. All mammals have four different sodium pump sub- types, or isoforms, that each has unique properties and tissue expression patterns.[1]This was investigated by following the passage of radioactively labeled ions across the plasma membrane of certain cells. It was found that the concentrations of sodium and potassium ions on the two sides of the membrane are interdependent, suggesting that the same carrier transports both ions. It is now known that the carrier is an ATP- ase and that it pumps three sodium ions out of the cell for every two potassium ions pumped in. The sodium- potassium pump was discovered in the 1. Danish scientist, Jens Christian Skou, who was awarded a Nobel Prize in 1. It marked an important step forward in the understanding of how ions get into and out of cells, and it has a particular significance for excitable cells such as nervous cells, which depend on this pump for responding to stimuli and transmitting impulses. Function[edit]The Na+/K+- ATPase helps maintain resting potential, effect transport, and regulate cellular volume.[2] It also functions as a signal transducer/integrator to regulate MAPK pathway, ROS, as well as intracellular calcium. In most animal cells, the Na+/K+- ATPase is responsible for about 1/5 of the cell's energy expenditure.[citation needed] For neurons, the Na+/K+- ATPase can be responsible for up to 2/3 of the cell's energy expenditure.[3]Resting potential[edit]. The Na+/K+- ATPase, as well as effects of diffusion of the involved ions maintain the resting potential across the membranes. Sodium Chloride 0.9% Intravenous Infusion BP - Summary of Product Characteristics (SPC) by Baxter Healthcare Ltd.
In order to maintain the cell membrane potential, cells keep a low concentration of sodium ions and high levels of potassium ions within the cell (intracellular). The sodium- potassium pump mechanism moves 3 sodium ions out and moves 2 potassium ions in, thus, in total, removing one positive charge carrier from the intracellular space. Please see Mechanism for details). Transport[edit]Export of sodium from the cell provides the driving force for several secondary active transporters membrane transport proteins, which import glucose, amino acids, and other nutrients into the cell by use of the sodium gradient. Another important task of the Na+- K+ pump is to provide a Na+ gradient that is used by certain carrier processes. In the gut, for example, sodium is transported out of the reabsorbing cell on the blood (interstitial fluid) side via the Na+- K+ pump, whereas, on the reabsorbing (lumenal) side, the Na+- glucose symporter uses the created Na+ gradient as a source of energy to import both Na+ and glucose, which is far more efficient than simple diffusion. Similar processes are located in the renal tubular system. Controlling cell volume[edit]Failure of the Na+- K+ pumps can result in swelling of the cell. A cell's osmolarity is the sum of the concentrations of the various ion species and many proteins and other organic compounds inside the cell. When this is higher than the osmolarity outside of the cell, water flows into the cell through osmosis. This can cause the cell to swell up and lyse. The Na+- K+ pump helps to maintain the right concentrations of ions. Furthermore, when the cell begins to swell, this automatically activates the Na+- K+ pump.[citation needed]Functioning as signal transducer[edit]Within the last decade [when?], many independent labs have demonstrated that, in addition to the classical ion transporting, this membrane protein can also relay extracellular ouabain- binding signalling into the cell through regulation of protein tyrosine phosphorylation. The downstream signals through ouabain- triggered protein phosphorylation events include activation of the mitogen- activated protein kinase (MAPK) signal cascades, mitochondrial reactive oxygen species (ROS) production, as well as activation of phospholipase C (PLC) and inositol triphosphate (IP3) receptor (IP3. R) in different intracellular compartments.[4]Protein- protein interactions play a very important role in Na+- K+ pump- mediated signal transduction. For example, Na+- K+ pump interacts directly with Src, a non- receptor tyrosine kinase, to form a signaling receptor complex.[5] Src kinase is inhibited by Na+- K+ pump, while, upon ouabain binding, the Src kinase domain will be released and then activated. Based on this scenario, Na. Ktide, a peptide Src inhibitor derived from Na+- K+ pump, was developed as a functional ouabain- Na+- K+ pump- mediated signal transduction.[6]Na+- K+ pump also interacts with ankyrin, IP3. R, PI3. K, PLC- gamma and cofilin.[7]Controlling neuron activity states[edit]The Na+- K+ pump has been shown to control and set the intrinsic activity mode of cerebellar. Purkinje neurons[8], accessory olfactory bulb mitral cells[9] and probably other neuron types[1. This suggests that the pump might not simply be a homeostatic, "housekeeping" molecule for ionic gradients; but could be a computation element in the cerebellum and the brain.[1. Indeed, a mutation in the Na+- K+ pump causes rapid onset dystonia parkinsonism, which has symptoms to indicate that it is a pathology of cerebellar computation.[1. Furthermore, an ouabain block of Na+- K+ pumps in the cerebellum of a live mouse results in it displaying ataxia and dystonia.[1. Alcohol inhibits sodium- potassium pumps in the cerebellum and this is likely how it corrupts cerebellar computation and body co- ordination.[1. The distribution of the Na+- K+ pump on myelinated axons, in human brain, was demonstrated to be along the internodal axolemma, and not within the nodal axolemma as previously thought.[1. Mechanism[edit]. The sodium–potassium exchange pump. The pump, after binding ATP, binds 3 intracellular Na+ ions.[2]ATP is hydrolyzed, leading to phosphorylation of the pump at a highly conserved aspartate residue and subsequent release of ADP. A conformational change in the pump exposes the Na+ ions to the outside. The phosphorylated form of the pump has a low affinity for Na+ ions, so they are released. The pump binds 2 extracellular K+ ions. This causes the dephosphorylation of the pump, reverting it to its previous conformational state, transporting the K+ ions into the cell. The unphosphorylated form of the pump has a higher affinity for Na+ ions than K+ ions, so the two bound K+ ions are released. ATP binds, and the process starts again. Regulation[edit]Endogenous[edit]The Na+/K+- ATPase is upregulated by c. AMP.[1. 7] Thus, substances causing an increase in c. AMP upregulate the Na+/K+- ATPase. These include the ligands of the Gs- coupled GPCRs. In contrast, substances causing a decrease in c. AMP downregulate the Na+/K+- ATPase. These include the ligands of the Gi- coupled GPCRs. Note: Early studies indicated the opposite effect, but these were later found to be inaccurate due to additional complicating factors.[citation needed]Exogenous[edit]The Na+- K+- ATPase can be pharmacologically modified by administrating drugs exogenously. Sodium Chloride 0. Intravenous Infusion BP - Summary of Product Characteristics (SPC)Sodium Chloride 0. Intravenous Infusion BPSodium chloride: 9. Each ml contains 9 mg sodium chloride. Na+ : 1. 54 Cl- : 1. H: 4,5 - 7. For the full list of excipients: see section 6. Solution for infusion. Clear solution, free from visible particles. Sodium Chloride 0. Treatment of isotonic extracellular dehydration. Treatment of sodium depletion. Vehicle or diluent of compatible drugs for parenteral administration. Posology. Adults, older people and children: Doses may be expressed in terms of m. Eq or mmol of sodium, mass of sodium, or mass of sodium salt (1 g Na. Cl = 3. 94 mg, 1. Eq or 1. 7. 1 mmol of Na and Cl). The dosage, rate and duration of administration is to be individualised as determined by several factors including age, weight, clinical condition, concomitant treatment and in particular the patient's hydration state, clinical and laboratory response to treatment. Fluid balance and plasma electrolyte concentrations must be monitored during treatment. Recommended dosage. The recommended dosage for treatment of isotonic extracellular dehydration and sodium depletion is. For adults : 5. 00 ml to 3 litres/2. For babies and children: 2. The recommended dosage when used as a vehicle or diluent ranges from 5. When Sodium Chloride 0. Method of administration. The solution is for administration by intravenous infusion through a sterile and non- pyrogenic administration set, using aseptic technique. The equipment should be primed with the solution in order to prevent air entering the system. The product should be inspected visually for particulate matter and discoloration prior to administration. Do not administer unless solution is clear, free from visible particles and the seal is intact. Do not remove unit from overwrap until ready for use. The inner bag maintains the sterility of the solution. Administer immediately following the insertion of infusion set. Do not connect flexible plastic containers in series in order to avoid air embolism due to possible residual air contained in the primary container. Pressurizing intravenous solutions contained in flexible plastic containers to increase flow rates can result in air embolism if the residual air in the container is not fully evacuated prior to administration. Use of a vented intravenous administration set with the vent in the open position could result in air embolism. Vented intravenous administration sets with the vent in the open position should not be used with flexible plastic containers. Additives may be introduced before infusion or during infusion through the injection site. For information on incompatibilities and preparation of the product (with additives), please see sections 6. The solution is contra- indicated in patient presenting hypernatraemia or hyperchloraemia. The contra- indications related to the added medicinal product should be considered. Fluid balance/renal function. Use in patients with (severe) renal impairment. Sodium Chloride 0. In such patients, administration of Sodium Chloride 0. See “Use in patients at risk for sodium retention, fluid overload and oedema” below; for additional considerations.)Risk of fluid and/or solute overload and electrolyte disturbances. Depending on the volume and rate of infusion, intravenous administration of Sodium Chloride 0. Fluid and/or solute overload resulting in overhydration/hypervolemia and, for example, congested states, including central and peripheral oedema. Clinically relevant electrolyte disturbances and acid- base imbalance. In general, the risk of dilutional states (retention of water relative to sodium) is inversely proportional to the electrolyte concentrations of Sodium Chloride 0. Conversely, the risk of solute overload causing congested states (retention of solute relative to water) is directly proportional to the electrolyte concentrations of Sodium Chloride 0. Special clinical monitoring is required at the beginning of any intravenous infusion. Clinical evaluation and periodic laboratory determinations may be necessary to monitor changes in fluid balance, electrolyte concentrations, and acid- base balance during prolonged parenteral therapy or whenever the condition of the patient or the rate of administration warrants such evaluation. Use in patients at risk for sodium retention, fluid overload and oedema. Sodium Chloride 0. Hypernatraemia. Rapidly correcting hypernatraemia once adaptation has occurred may lead to cerebral oedema, potentially resulting in seizures, permanent brain damage, or death. Hyperchloraemia. • Metabolic acidosis, which may be worsened by prolonged use of this product, especially in patients with renal impairment. Hypervolaemia such as congestive heart failure and pulmonary oedema may be precipitated, particularly in patients with cardiovascular disease. Iatrogenic hyperchloraemic metabolic acidosis (e. Conditions that may cause sodium retention, fluid overload and oedema (central and peripheral), such as patients witho primary hyperaldosteronism,o secondary hyperaldosteronism, associated with, for example,- hypertension,- congestive heart failure,- liver disease (including cirrhosis),- renal disease (including renal artery stenosis, nephrosclerosis) or pre- eclampsia. Medications that may increase the risk of sodium and fluid retention, such as corticosteroids. Infusion reactions. Symptoms of unknown aetiology which can appear to be hypersensitivity reactions have been reported very rarely in association with infusion of Sodium Chloride 0. These have been characterized as hypotension, pyrexia, tremor, chills, urticaria, rash and pruritus. Stop the infusion immediately if signs or symptoms of these reactions develop. Appropriate therapeutic countermeasures should be instituted as clinically indicated. Specific patient groups. The consulting physician should be experienced in this product's use and safety in these special populations that are especially sensitive to rapid changes in serum sodium levels. Rapid correction of hyponatraemia and hypernatraemia is potentially dangerous (risk of serious neurologic complications). See section “Hyponatraemia/hypernatraemia” above. Paediatric population. Plasma electrolyte concentrations should be closely monitored in the paediatric population as this population may have impaired ability to regulate fluids and electrolytes. Repeated infusions of sodium chloride should therefore only be given after determination of the serum sodium level. Geriatric population. When selecting the type of infusion solution and the volume/rate of infusion for a geriatric patient, consider that geriatric patients are generally more likely to have cardiac, renal, hepatic, and other diseases or concomitant drug therapy. For information on preparation of the product and additives, please see section 6. Caution is advised in patients treated with lithium. Renal sodium and lithium clearance may be increased during administration of Sodium Chloride 0. Administration of Sodium Chloride 0. Corticoids/Steroids and carbenoxolone, are associated with the retention of sodium and water (with oedema and hypertension). See Section 4. 4 Special warnings and precautions for use. There are no adequate data from the use of Sodium Chloride 0. The physician should carefully consider the potential risks and benefits for each specific patient before administering Sodium Chloride 0. Caution is advised with patients with pre- eclampsia (See Section 4. Special warnings and precautions for use). When a medicinal product is added, the nature of the drug and its use during pregnancy and lactationhas to be considered separately. No studies have been conducted on the influence of Sodium Chloride 0. The following adverse reactions have been reported in post- marketing experience. The frequency of the adverse drug reactions listed in this section cannot be estimated from the available data. System Organ Class (SOC)Adverse reactions (Preferred Term)Frequency. Nervous system disorders. Tremor. Not known. Vascular disorders. Hypotension. Not known. Skin and subcutaneous tissue disorders. Urticaria. Rash. Pruritus. 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