Extracellular fluid sodium

Sodium is the most abundant extracellular cation in the body and is the major osmotically active ion in the extracellular fluid. Sodium concentration determines the distribution of... 

Despite the higher level of sodium 111 natural water, potassium is universally the characteristic cation found within both plant and animal cells. Although sodium is not an absolute requirement for most plants and bacteria, it is found in these organisms and is essential to higher animals where it is the principal cation of the extracellular fluids. Sodium and potassium are important constituents of both ultra- and extracellular fluids. Generally, the best external and internal medium for function of cells not adjusted to low salt levels is a medium involving a balance of sodium and potassium. 

Interest in the use of ion-selective electrodes in the biomedical field is a natural consequence of the electrolyte composition of bulk body and cell fluids (Table 2.1), a proportion of which is in the ionised form. In extracellular fluids, sodium is the principal cation with chloride as the major anion. In intracellular fluids, potassium is the major cation and phosphate the principal anion — except in erythrocytes where chloride predominates. Of special interest is ionised calcium, because of its importance in various physiological and biochemical processes such as bone formation, nerve conduction, cerebral function, cardiac conduction and contraction, membrane phenomena, muscle contraction and relaxation, blood coagulation, and enzyme activation [2—4]. 

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. 

The volume of extracellular fluid is direcdy related to the Na" concentration which is closely controlled by the kidneys. Homeostatic control of Na" concentration depends on the hormone aldosterone. The kidney secretes a proteolytic enzyme, rennin, which is essential in the first of a series of reactions leading to aldosterone. In response to a decrease in plasma volume and Na" concentration, the secretion of rennin stimulates the production of aldosterone resulting in increased sodium retention and increased volume of extracellular fluid (51,55). 

Hyperaldosteronism is a syndrome caused by excessive secretion of aldosterone. It is characterized by renal loss of potassium. Sodium reabsorption in the kidney is increased and accompanied by an increase in extracellular fluid. Clinically, an increased blood pressure (hypertension) is observed. Primary hyperaldosteronism is caused by aldosterone-producing, benign adrenal tumors (Conn s syndrome). Secondary hyperaldosteronism is caused by activation of the renin-angiotensin-aldosterone system. Various dtugs, in particular diuretics, cause or exaggerate secondary peadosteronism. 

The extracellular fluid (ECF) is the fluid outside the cell and is rich in sodium, chloride, and bicarbonate. O The ECF is approximately one-third of TBW (14 L in a 70-kg man or 12 Lin a 70-kg woman) and is subdivided into two compartments the interstitial fluid and the intravascular fluid. The interstitial fluid (also known as lymphatic fluid) represents the fluid occupying the spaces between cells, and is about 25% of TBW (10.5 L in a 70-kg man or 8.8 L in a 70-kg woman). The intravascular fluid (also known as plasma) represents the fluid within the blood vessels and is about 8% of TBW (3.4 L in a 70-kg man or 2.8 L in a 70-kg woman). The ECF is approximately one-third of TBW or 14 L in a 70-kg male. Because the exact percentages are cumbersome to recall, many clinicians accept that the ECF represents roughly 20% of body weight (regardless of gender) with 15% in the interstitial space and 5% in the intravascular space.6 Note that serum electrolytes are routinely measured from the ECF. 

The mainstay of treatment for established SOS is supportive care aimed at sodium restriction, increasing intravascular volume, decreasing extracellular fluid accumulation, and minimizing factors that contribute to or exacerbate hepatotoxicity and encephalopathy. Defibrotide has shown promising results in the treatment of SOS.44... 

Aldosterone acts on the distal tubule of the nephron to increase sodium reabsorption. The mechanism of action involves an increase in the number of sodium-permeable channels on the luminal surface of the distal tubule and an increase in the activity of the Na+-K+ ATPase pump on the basilar surface of the tubule. Sodium diffuses down its concentration gradient out of the lumen and into the tubular cells. The pump then actively removes the sodium from cells of the distal tubule and into the extracellular fluid so that it may diffuse into the surrounding capillaries and return to the circulation. Due to its osmotic effects, the retention of sodium is accompanied by the retention of water. In other words, wherever sodium goes, water follows. As a result, aldosterone is very important in regulation of blood volume and blood pressure. The retention of sodium and water expands the blood volume and, consequently, increases mean arterial pressure. 

Diuretics are a group of therapeutic agents designed to reduce the volume of body fluids. Their mechanism of action is at the level of the kidney and involves an increase in the excretion of Na+ and Cl ions and, consequently, an increase in urine production. As discussed in Chapter 2, sodium is the predominant extracellular cation and, due to its osmotic effects, a primary determinant of extracellular fluid volume. Therefore, if more sodium is excreted in the urine, then more water is also lost, thus reducing the volume of extracellular fluids including the plasma. 

Osmotic diuretics such as mannitol act on the proximal tubule and, in particular, the descending limb of the Loop of Henle — portions of the tubule permeable to water. These drugs are freely filtered at the glomerulus, but not reabsorbed therefore, the drug remains in the tubular filtrate, increasing the osmolarity of this fluid. This increase in osmolarity keeps the water within the tubule, causing water diuresis. Because they primarily affect water and not sodium, the net effect is a reduction in total body water content more than cation content. Osmotic diuretics are poorly absorbed and must be administered intravenously. These drugs may be used to treat patients in acute renal failure and with dialysis disequilibrium syndrome. The latter disorder is caused by the excessively rapid removal of solutes from the extracellular fluid by hemodialysis. 

Sodium is the major extracellular cation. Because of its osmotic effects, changes in sodium content in the body have an important influence on extracellular fluid volume, including plasma volume. For example, excess sodium leads to the retention of water and an increase in plasma volume. Increased plasma volume then causes an increase in blood pressure. Conversely, sodium deficit leads to water loss and decreased plasma volume. A decrease in plasma volume then causes a decrease in blood pressure. Therefore, homeostatic mechanisms involved in the regulation of plasma volume and blood pressure involve regulation of sodium content, or sodium balance, in the body. 

Regulation of the osmolarity of extracellular fluid, including that of the plasma, is necessary in order to avoid osmotically induced changes in intracellular fluid volume. If the extracellular fluid were to become hypertonic (too concentrated), water would be pulled out of the cells if it were to become hypotonic (too dilute), water would enter the cells. The osmolarity of extracellular fluid is maintained at 290 mOsm/1 by way of the physiological regulation of water excretion. As with sodium, water balance in the body is achieved when water intake is equal to water output. Sources of water input include ... 

Ca2+ is necessary for transmission at the neuromuscular junction and other synapses and plays a special role in exocytosis. In most cases in the CNS and PNS, chemical transmission does not occur unless Ca2+ is present in the extracellular fluid. Katz and Miledi [16] elegantly demonstrated the critical role of Ca2+ in neurotransmitter release. The frog NMJ was perfused with salt solution containing Mg2+ but deficient in Ca2+. A twin-barrel micropipet, with each barrel filled with 1.0mmol/l of either CaCl2 or NaCl, was placed immediately adjacent to the terminal. The sodium barrel was used to depolarize the nerve terminal electrically and the calcium barrel to apply Ca2+ ionotophoretically. Depolarization without Ca2+ failed to elicit an EPP (Fig. 10-6A). If Ca2+ was applied just before the depolarization, EPPs were evoked (Fig. 10-6B). In contrast, EPPs could not be elicited if the Ca2+ pulse immediately followed the depolarization (Fig. 10-6C). EPPs occurred when a Ca2+ pulse as short as 1 ms preceded the start of the depolarizing pulse by as little as 50-100 (xs. The experiments demonstrated that Ca2+ must be present when a nerve terminal is depolarized in order for neurotransmitter to be released. 

Acutely, diuretics lower BP by causing diuresis. The reduction in plasma volume and stroke volume associated with diuresis decreases cardiac output and, consequently, BP. The initial drop in cardiac output causes a compensatory increase in peripheral vascular resistance. With chronic diuretic therapy, the extracellular fluid volume and plasma volume return almost to pretreatment levels, and peripheral vascular resistance falls below its pretreatment baseline. The reduction in peripheral vascular resistance is responsible for the long-term hypotensive effects. Thiazides lower BP by mobilizing sodium and water from arteriolar walls, which may contribute to decreased peripheral vascular resistance. 

Despite their successful use for at least 20 years, the mechanisms by which they lower the blood pressure remain uncertain. Theories to explain the antihypertensive effectiveness of the diuretic agents have included a) alteration of sodium and water content on arterial smooth muscle, b) the induction of a decreased vascular response to catecholamines, c) a decrease in blood volume and total extracellular fluid volume, and d) a direct vasodilator action independent from the diuretic effect(12). 

The basic answer to this question is that ions move across the plasma membrane of the neuron. Recall that ions are charged particles, frequently derived from single atoms by the gain or loss of electrons. The ions that are most important to us in understanding nervous system function are sodium ion, Na+, potassium ion, K+, calcium ion, Ca +, and chloride ion, Cl . If we compare the concentrations of these ions on the inside of the neuron and in the extracellular fluid that bathes the neuron, we find the neuron interior has a higher concentration of potassium ion than does the exterior fluid. In contrast, the exterior fluid has higher concentrations of sodium, calcium, and chloride ions than does the neuron interior. These concentration differences are referred to as concentration gradients. 

Sodium chloride (normal saline)- 0.9% Sodium chloride (normal saline), which is isotonic, restores both water and sodium chloride losses. Other indications for parenteral 0.9% saline include Diluting or dissolving drugs for IV, IM, or subcutaneous injection flushing of IV catheters extracellular fluid replacement treatment of metabolic alkalosis in the presence of fluid loss and mild sodium depletion as a priming solution in hemodialysis procedures and to initiate and terminate blood transfusions without hemolyzing red blood cells. 

Pharmacology Normal osmolarity of the extracellular fluid ranges between 280 to 300 mOsm/L it is primarily a function of sodium and its accompanying ions, chloride, and bicarbonate. Sodium chloride is the principal salt involved in maintenance of plasma tonicity. One gram of sodium chloride provides 17.1 mEg sodium and 17.1 mEq chloride. 

Pharmacokinetics Sodium bicarbonate in water dissociates to provide sodium and bicarbonate ions. Sodium is the principal cation of extracellular fluid. Bicarbonate is a normal constituent of body fluids and normal plasma level ranges from 24 to 31 mEq/L. Plasma concentration is regulated by the kidney. Bicarbonate anion is considered labile because, at a proper concentration of hydrogen ion, it may be converted to carbonic acid, then to its volatile form, carbon dioxide, excreted by lungs. Normally, a ratio of 1 20 (carbonic acid bicarbonate) is present in extracellular fluid. In a healthy adult with normal kidney function, almost all the glomerular filtered bicarbonate ion is reabsorbed less than 1% is excreted in urine. 

Potassium, along with nitrogen and phosphorus, is an essential element needed for plant growth. In plants, it occurs mostly as K+ ion in cell juice. It is found in fruit or seed. Deficiency can cause curling leaves, yellow or brown coloration of leaves, weak stalk and diminished root growth. Potassium deficiency has been associated with several common animal ailments. Potassium is in extracellular fluid in animals at lower concentrations than sodium. 

Body fluids are partitioned between the intracellular fluids (ICF), which constitute two-thirds of total body water, and extracellular fluids (ECF), which constitute one-third of total body water. The ECF consists of plasma and interstitial fluid plus lymph. The ionic composition differs substantially between ECF and ICF (Table 21.1). Sodium is the primary cation in ECF, whereas potassium is the principal intracellular cation. 

Fluoride taken in the form of sodium fluoride as a tablet or solution is absorbed rapidly. Only a few minutes after intake, there is a rise in plasma fluoride. The fluctuation in plasma fluoride concentration is dependent on the fluoride dose ingested, the dose frequency and the plasma half-life of fluoride. The half time for absorption is --30 min, so peak plasma concentration usually occurs within 30-60 min [64-69]. Absorbed fluoride is rapidly distributed by the circulation to the intracellular and extracellular fluids and is retained only in calcified tissues. The sensitivity of the serum fluoride concentrations to previous intake, glomerular filtration and the intensity of bone resorption suggests that the human organism exerts no direct homeostatic control and that fluoride concentrations reflect the recent intake [73]. Plasma fluoride levels increase with age, with increasing fluoride content of bone and as a consequence of renal insufficiency [2]. 

Mechanism of Action A sulfonamide derivative that acts as a thiazide diuretic and antihypertensive. As a diuretic, blocks reabsorption of water and the electrolytes sodium and potassium at cortical diluting segment of distal tubule. As an antihypertensive, reduces plasma and extracellular fluid volume, decreases peripheral vascular resistance (PVR) by direct effect on blood vessels. Therapeutic Effect Promotes diuresis, reduces BP. 

Mechanism of Action A thiazide diuretic that blocks reabsorption of sodium, potassium, and water at the distal convoluted tubule also decreases plasma and extracellular fluid volume and peripheral vascular resistance. Therapeutic Effect Produces diuresis lowers BP. 

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