Sodium potassium ATPase

The kidney contains the major site of renin synthesis, the juxtaglomerular cells in the wall of the afferent arteriole. From these cells, renin is secreted not only into the circulation but also into the renal interstitium. Moreover, the enzyme is produced albeit in low amounts by proximal tubular cells. These cells also synthesize angiotensinogen and ACE. The RAS proteins interact in the renal interstitium and in the proximal tubular lumen to synthesize angiotensin II. In the proximal tubule, angiotensin II activates the sodium/hydrogen exchanger (NHE) that increases sodium reabsorption. Aldosterone elicits the same effect in the distal tubule by activating epithelial sodium channels (ENaC) and the sodium-potassium-ATPase. Thereby, it also induces water reabsotption and potassium secretion. 

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Maier WE, Costa LG. 1990. Sodium, potassium-ATPase in rat brain and erythrocytes as a possible target and marker, respectively, for neurotoxicity studies with chlordecone, organotins and mercury compounds. Toxicol Lett 51 175-188. 

Sodium, potassium ATPase HIV reverse transcriptase Steroid 5a-reductase... 

Pumps move ions and molecules up their electrochemical gradient. Pumps require energy, usually in the form of ATP hydrolysis. Sodium-potassium ATPase is an example of a pump. Cells maintain a higher concentration of potassium inside the cell than they do outside the cell. Sodium is maintained low inside, high outside. Sodium-potassium ATPase pumps three sodium ions from inside the cell to outside. This is the unfavorable direction—Na+ moves from low concentration to a higher one and against the membrane potential. At the same time, it also... 

Glitsch, H. G. Electrophysiology of the sodium-potassium -ATPase in cardiac cells. Physiol. Rev. 81 1791-1826,2001. 

Singh AP, Shanker K, Parvez SH. 1984. Effect of Kepone on catecholamine-stimulated sodium, potassium-ATPase of rat brain. Biogenic Amines 1 (4) 313-318. 

ATP is used not only to power muscle contraction, but also to re-establish the resting state of the cell. At the end of the contraction cycle, calcium must be transported back into the sarcoplasmic reticulum, a process which is ATP driven by an active pump mechanism. Additionally, an active sodium-potassium ATPase pump is required to reset the membrane potential by extruding sodium from the sarcoplasm after each wave of depolarization. When cytoplasmic Ca2- falls, tropomyosin takes up its original position on the actin and prevents myosin binding and the muscle relaxes. Once back in the sarcoplasmic reticulum, calcium binds with a protein called calsequestrin, where it remains until the muscle is again stimulated by a neural impulse leading to calcium release into the cytosol and the cycle repeats. 

Fig. 1 Thyroid hormone synthesis in a thyroid follicular cell. NIS and TPO (organification and coupling reaction) have been marked in red dashed line as the two main targets for direct thyroid gland function disrupters. DEHALl iodotyrosine dehalogenase 1, DIT diiodotyrosine, DUOX2 dual oxidase 2, MIT monoiodotyrosine, Na/K-ATPase sodium-potassium ATPase, NIS sodium-iodide symporter, PSD pendrin, TG thyroglobulin, TPO thyroperoxidase. Reprinted from [7] with permission from Elsevier...

Nerve stimulation results in a net influx of sodium ions, and normal conditions are restored by the outward transport of sodium ions against an electrochemical gradient. While several earlier workers had identified ATPases in the sheath of giant squid axons, it was Skou who first connected the sodium, potassium ATPase [EC 3.6.1.37] with the ion flux of neurons. This discovery culminated... 

Amiloride and triamterene-Am or 6e and triamterene not only inhibit sodium reabsorption induced by aldosterone, but they also inhibit basal sodium reabsorption. They are not aldosterone antagonists, but act directly on the renal distal tubule, cortical collecting tubule and collecting duct. They induce a reversal of polarity of the transtubular electrical-potential difference and inhibit active transport of sodium and potassium. Amiloride may inhibit sodium, potassium-ATPase. 

Parenteral /32-agonists such as albuterol (salbuta-mol) increase the activity of the membrane sodium-potassium ATPase, and so increase potassium entry into cells. Nebulized or infused albuterol (salbutamol) significantly lowers serum potassium concentration over 5 hours. A suitable initial dose of nebulized albuterol is 5 mg in adults. It can provoke tremor and tachyarrhythmia, and it is desirable to monitor cardiac rhythm during nebulization. The combination of nebulized albuterol (salbutamol) with infusion of insulin + glucose is more effective than the infusion alone. 

Mechanism of Action A potassium-sparing diuretic that inhibits sodium, potassium, ATPase. Interferes with sodium and potassium exchange in distal tubule, cortical col-lectingtubule, and collecting duct. Increases sodium and decreases potassium excretion. Also increases magnesium, decreases calcium loss. TAerapeuticEffect Produces diuresis and lowers BP. 

Inorganic ions, such as sodium and potassium, move through the cell membrane by active transport. Unlike diffusion, energy is required for active transport as the chemical is moving from a lower concentration to a higher one. One example is the sodium-potassium ATPase pump, which transports sodium [Na ] ions out of the cell and potassium [K ] into the cell. 

This must obviously be the opposite of passive transport. Active transport does require energy, usually in the form of the consumption of ATP or GTP, because the molecules are moving against the concentration gradient from an area of lower concentration to an area of higher concentration. The most well known active transport system is the Sodium-Potassium-ATPase Pump (Na" "- K+ZATPase) which maintains an imbalance of sodium and potassium ions inside and outside the membrane, respectively. See Figure 3. 

Sodium-Potassium ATPase Pump An Active Transport System... 

One example of molecular transport requiring energy is the reuptake of neurotransmitter into its presynaptic neuron, as already mentioned above. In this case, the energy comes from linkage to an enzyme known as sodium-potassium ATPase (Fig. 2—9). An active transport pump is the term for this type of organization of two neurotransmitters, namely a transport carrier and an energy-providing system, which function as a team to accomplish transport of a molecule into the cell (Fig. 2—11). 

Cardiac glycosides cause a positive inotropic effect which means an increase of the cardiac beat volume by enhanced contraction ability. The reason for this is supposed to be aligned with the direct inhibition of the transport enzyme sodium/ potassium-ATPase. The decrease of sodium ions enhances the calcium ion concentration, which activates the myofibrillic enzyme and inactivates proteins like tropo-myocine and tropomine. Till present, a final proof for this hypothesis is lacking, the toxicity, however, is definitely aligned with these effects [97]. 

Lees G. J. (1991). Inhibition of sodium-potassium-ATPase a potentially ubiquitous mechanism contributing to central nervous system neuropathology. Brain Res Brain Res Rev. 16 283-300. 

Extrapolating from well-characterized enzymatic inhibition in test tubes, numerous mechanistic ideas concerning the in vivo effects of vanadium compounds have been advanced. The effects of vanadium compounds as transition-state analogs of certain enzymes with a phosphoprotein intermediate in their reaction scheme is proposed to account for the action of vanadium [11] in many biological systems. Unfortunately, it is often difficult to determine if the inhibition observed in the test tube occurs in vivo. For example, although vanadate is a potent inhibitor of plasma membrane ion pumps (such as the sodium potassium ATPase) in the test tube, it is difficult to determine if these pumps are actually inhibited in animals exposed to vanadium compounds. Currently, the role of vanadium compounds as protein phosphatase (PTP) inhibitors is believed to be related to the metabolic effects of this... 

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