Sodium intracellular

Sodium and Potassium. Whereas sodium ion is the most abundant cation in the extracellular fluid, potassium ion is the most abundant in the intracellular fluid. Small amounts of K" are requited in the extracellular fluid to maintain normal muscle activity. Some sodium ion is also present in intracellular fluid (see Fig. 5). Common food sources rich in potassium may be found in Table 7. Those rich in sodium are Hsted in Table 8. 

Active Transport. Maintenance of the appropriate concentrations of K" and Na" in the intra- and extracellular fluids involves active transport, ie, a process requiring energy (53). Sodium ion in the extracellular fluid (0.136—0.145 AfNa" ) diffuses passively and continuously into the intracellular fluid (<0.01 M Na" ) and must be removed. This sodium ion is pumped from the intracellular to the extracellular fluid, while K" is pumped from the extracellular (ca 0.004 M K" ) to the intracellular fluid (ca 0.14 M K" ) (53—55). The energy for these processes is provided by hydrolysis of adenosine triphosphate (ATP) and requires the enzyme Na" -K" ATPase, a membrane-bound enzyme which is widely distributed in the body. In some cells, eg, brain and kidney, 60—70 wt % of the ATP is used to maintain the required Na" -K" distribution. 

Intake of a large amount of sodium chloride negates the antihypertensive effects of diuretics. Other mechanisms, such as direct vasodilating action, decreased responsiveness to vasopressor agents, stimulation of prostacyclin [35121 -78-9] production, and reduction in the intracellular calcium... 

Oblimersen sodium is a DNA antisense oligonucleotide designed to specifically bind to human bcl-2 mRNA, resulting in catalytic degradation of bcl-2. This results in decreased translation of the protein Bcl-2, which is a cellular antiapoptotic protein. Thus, oblimersen enhances sensitivity to chemotherapy by shifting the intracellular balance to a state in which the cells are more likely to be killed by apoptosis. Currently, it is used in combination chemotherapy for treating advanced melanoma. 

Additional cellular events linked to the activity of blood pressure regulating substances involve membrane sodium transport mechanisms Na+/K.+ ATPase Na+fLi countertransport Na+ -H exchange Na+-Ca2+ exchange Na+-K+ 2C1 transport passive Na+ transport potassium channels cell volume and intracellular pH changes and calcium channels. 

Inhibition of the Na+/K+-ATPase leads to a loss of potassium and an increase of sodium within the cell. Secondary intracellular calcium is increased via the Na VCa -exchanger. This results in a positive inotropic effect in the myocardium, with an increase of peak force and a decrease in time to peak tension. Besides this, cardiac glycosides increase vagal activity by effects on the central vagal nuclei, the nodose ganglion and increase in sensitivity of the sinus node to acetylcholine. 

The main endogenous mineralocorticoid is aldosterone, which is mainly produced by the outer layer of the adrenal medulla, the zonaglomerulosa. Aldostorone, like other steroids, binds to a specific intracellular (nuclear) receptor, the mineralocorticoid receptor (MR). Its main action is to increase sodium reabsotption by an action on the distal tubules in the kidney, which is accompanied by an increased excretion of potassium and hydrogen ions. 

Acute over-activation of NHE1 results in a marked elevation in intracellular sodium concentration with a subsequent increase in intracellular calcium, via the Na +/Ca++ exchanger. This in turn triggers a cascade of injurious events that can culminate in tissue dysfunction and ultimately apoptosis and necrosis. This is commonly seen in organs such as the heart, brain and kidneys as a consequence of ischemia-reperfusion. 

Juel, C. (1988), Intracellular pH recovery and lactate efflux in mouse soleus muscles stimulated in vitro The involvement of sodium/proton exchange and a lactate carrier. Acta Physiol. Scand. 132,... 

Confirmation that FMLP-induced activation involves release of intracellular calcium was obtained by loading neutrophils with CTC. Addition of 20 pH CTC to a neutrophil suspension resulted in a gradual increase in CTC fluorescence as the probe entered the cells and partitioned into intracellular membranes (Figure 9, upper panel). Addition of FMLP resulted in an abrupt decrease in fluorescence, suggesting release of calcium from intracellular membranes probed by CTC. The FMLP-induced release of calcium monitored by CTC was little affected by increased medium osmolality a similar fluorescence decrease was seen in the presence of sodium HEPES (645 mosmol/kg) or sodium sulfate (662 mosmol/kg) (Figure 9, lower panel). 

Involved in membrane function principal cations of extracellular-and intracellular fluids, respectively Sodium, potassium... 

Decreased cerebral blood flow, resulting from acute arterial occlusion, reduces oxygen and glucose delivery to brain tissue with subsequent lactic acid production, blood-brain barrier breakdown, inflammation, sodium and calcium pump dysfunction, glutamate release, intracellular calcium influx, free-radical generation, and finally membrane and nucleic acid breakdown and cell death. The degree of cerebral blood flow reduction following arterial occlusion is not uniform. Tissue at the... 

A number of studies in fact show clear Di effects. Intracellular recording from striatal neurons in rat brain slices show a cAMP-mediated Di-dependent (blocked by SCH 23390) suppression of a voltage-dependent sodium current which make the cell less responsive. 

A sustained inhibition of the Na/K pump following a period of oxidant stress would be expected to raise intracellular sodium and favour calcium influx via the Na/Ca exchanger. Ischaemia and reperflision-induced oxidant stress, therefore, may result in a loss of Na/K pump activity, an eflFect that may involve free-radical-mediated changes in cellular thiol status. 

Bers, D.M. and Ellis, D. (1982). Intracellular calcium and sodium activity in sheep heart Purkinje fibres. Effects of changes of external sodium and intracellular pH. Pflugers Arch. Eur. J. Physiol. 393, 171-178. 

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