Role of Kidneys In Regulation Of Potassium Levels In ECF

Extracellular fluid potassium concentration normally is regulated at about 4.2 mEq/L ±0.3 mEq/L More than 98 percent of the total body potassium is contained in the cells and only 2 percent is in the extracellular fluid Maintenance of balance between intake and output of potassium depends primarily on excretion by the kidneys because the amount excreted in the feces is only 5 to 10 percent of the potassium intake Redistribution of potassium between the intracellular and extracellular fluid compartments provides a first line of defense against changes in extracellular fluid potassium concentration

Regulation of Internal Potassium Distribution Insulin stimulates Potassium uptake into cells Aldosterone increases Potassium uptake into cells β-adrenergic stimulation increases cellular uptake of Potassium Metabolic acidosis increases extracellular potassium concentration Metabolic alkalosis decreases extracellular fluid potassium concentration Cell lysis causes increased extracellular potassium concentration

Strenuous exercise can Cause hyperkalemia by releasing Potassium from skeletal muscle Increased extracellular fluid osmolarity causes redistribution of Potassium from the cells to extracellular Fluid

About 65 percent of the filtered potassium is reabsorbed in the proximal tubule Another 25 to 30 percent of the filtered potassium is reabsorbed in the loop of Henle especially in the thick ascending part where potassium is actively co-transported along with sodium and chloride Most of the day-to-day regulation of potassium excretion occurs in the late distal and cortical collecting tubules, where potassium can be either reabsorbed or secreted, depending on the needs of the body

When potassium intake is low, the secretion rate of potassium in the distal and collecting tubules decreases causing reduction in urinary potassium secretion

Intercalated cells can reabsorb Potassium during Potassium depletion

The most important factors that stimulate potassium secretion by the principal cells include (1) increased extracellular fluid potassium concentration (2) increased aldosterone (3) increased tubular flow rate

Increased extracellular fluid potassium concentration raises potassium secretion by three mechanisms (1) Increased extracellular fluid potassium concentration stimulates the sodium-potassium ATPase pump (2) Increased extracellular potassium concentration increases the potassium gradient from the renal interstitial fluid to the interior of the epithelial cell; this reduces back leakage of potassium ions from inside the cells through the basolateral membrane

(3) Increased potassium concentration stimulates aldosterone secretion by the adrenal cortex which further stimulates potassium secretion by Stimulating sodium-potassium-ATPase pump By increasing the permeability of the luminal membrane for potassium

Increased Distal Tubular Flow Rate Stimulates Potassium Secretion A rise in distal tubular flow rate, as occurs with volume expansion, high sodium intake or treatment with some diuretics stimulates potassium secretion

The effect of tubular flow rate on potassium secretion in the distal and collecting tubules is strongly influenced by potassium intake When potassium intake is high, increased tubular flow rate has a much greater effect to stimulate potassium secretion than when potassium intake is low

The effect of increased tubular flow rate is important in helping to preserve normal potassium excretion during changes in sodium intake For example, with a high sodium intake, there is decreased aldosterone secretion, which by itself would tend to decrease the rate of potassium secretion and, therefore, reduce urinary excretion of potassium. However, the high distal tubular flow rate that occurs with a high sodium intake tends to increase potassium secretion The two effects of high sodium intake, decreased aldosterone secretion and the high tubular flow rate, counterbalance each other, so there is little change in potassium excretion

Acute increases in hydrogen ion concentration of the extracellular fluid (acidosis) reduce potassium secretion, whereas decreased hydrogen ion concentration (alkalosis) increases potassium secretion The primary mechanism by which increased hydrogen ion concentration inhibits potassium secretion is by reducing the activity of the sodium-potassium ATPase pump This in turn decreases intracellular potassium concentration and subsequent passive diffusion of potassium across the luminal membrane into the tubule Chronic acidosis leads to a loss of potassium whereas acute acidosis leads to decreased potassium excretion

Role Of Kidneys In Regulation Of Calcium Levels In ECF

Calcium excretion is adjusted to meet the body's needs With an increase in calcium intake there is also increased renal calcium excretion With calcium depletion calcium excretion by the kidneys decreases as a result of enhanced tubular reabsorption

About 65 percent of the filtered calcium is reabsorbed in the proximal tubule, 25 to 30 percent is reabsorbed in the loop of Henle, and 4 to 9 percent is reabsorbed in the distal and collecting tubules

Proximal Tubular Calcium Reabsorption Most of the calcium reabsorption in the proximal tubule occurs through the paracellular pathway, dissolved in water and carried with the reabsorbed fluid as it flows between the cells Only about 20% of proximal tubular calcium reabsorption occurs through the transcellular pathway in two steps: calcium diffuses from the tubular lumen into the cell down an electrochemical gradient due to the much higher concentration of calcium in the tubular lumen, compared with the epithelial cell cytoplasm and because the cell interior is negative relative to the tubular lumen calcium exits the cell across the basolateral membrane by a calcium-ATPase pump and by sodium-calcium counter-transporter

Loop of Henle and Distal Tubule Calcium Reabsorption In the loop of Henle calcium reabsorption is restricted to the thick ascending limb Approximately 50% of calcium reabsorption in the thick ascending limb occurs through the paracellular route by passive diffusion due to the slight positive charge of the tubular lumen relative to the interstitial fluid The remaining 50% of calcium reabsorption in the thick ascending limb occurs through the transcellular pathway, a process that is stimulated by PTH

In the distal tubule there is diffusion across the luminal membrane through calcium channels and exit across the basolateral membrane by a calcium-ATPase pump, as well as a sodium-calcium counter transport mechanism

Excretion Of Phosphate Renal phosphate excretion is controlled by an overflow mechanism when phosphate concentration in the plasma is below the critical value of about 1 mmol/L, all the phosphate in the glomerular filtrate is reabsorbed and no phosphate is lost in the urine But above this critical concentration, the rate of phosphate loss is directly proportional to the additional increase The proximal tubule normally reabsorbs 75 to 80 percent of the filtered phosphate The distal tubule reabsorbs about 10 percent of the filtered load, and only very small amounts are reabsorbed in the loop of Henle, collecting tubules, and collecting ducts Approximately 10 percent of the filtered phosphate is excreted in the urine

Control of Renal Magnesium Excretion and Extracellular Magnesium Ion Concentration More than one half of the body's magnesium is stored in the bones Most of the rest resides within the cells, with less than 1 percent located in the extracellular fluid The total plasma magnesium concentration is about 1.8 mEq/L, more than one half of this is bound to plasma proteins Therefore, the free ionized concentration of magnesium is only about 0.8 mEq/L

Renal excretion of magnesium can increase markedly during magnesium excess or decrease to almost nil during magnesium depletion The proximal tubule usually reabsorbs only about 25 percent of the filtered magnesium The primary site of reabsorption is the loop of Henle where about 65 percent of the filtered load of magnesium is reabsorbed Only a small amount (usually <5 percent) of the filtered magnesium is reabsorbed in the distal and collecting tubules

Pressure Natriuresis and Pressure Diuresis Pressure diuresis refers to the effect of increased blood pressure to raise urinary volume excretion Pressure natriuresis refers to the rise in sodium excretion with increased blood pressure

Sympathetic Nervous System Control of Renal Excretion The kidneys receive extensive sympathetic innervation changes in sympathetic activity can alter renal sodium and water excretion as well as extracellular fluid volume

When blood volume is reduced by hemorrhage there is reflex activation of the sympathetic nervous system This in turn increases renal sympathetic nerve activity which has several effects constriction of the renal arterioles with resultant decrease in GFR (2) increased tubular reabsorption of salt and water (3) stimulation of renin release and increased angiotensin II and aldosterone formation

Role of Angiotensin II in Controlling Renal Excretion When sodium intake is elevated above normal, renin secretion is decreased causing decreased angiotensin II formation Reduced level of angiotensin II decreases tubular reabsorption of sodium and water, thus increasing the kidneys' excretion of sodium and water The net result is to minimize the rise in extracellular fluid volume and arterial pressure that would otherwise occur when sodium intake increases

When sodium intake is reduced below normal, increased levels of angiotensin II cause sodium and water retention Changes in activity of the renin-angiotensin system act as a powerful amplifier of the pressure natriuresis mechanism for maintaining stable blood pressures and body fluid volumes

Role of Aldosterone in Controlling Renal Excretion Aldosterone increases sodium reabsorption, especially in the cortical collecting tubules. The increased sodium reabsorption is also associated with increased water reabsorption and potassium secretion

Role of ADH Water deprivation strongly elevates plasma levels of ADH that in turn increases water reabsorption by the kidneys and helps to minimize the decreases in extracellular fluid volume and arterial pressure

Role of Atrial Natriuretic Peptide in Controlling Renal Excretion The stimulus for release of this peptide is increased stretch of the atria which can result from excess blood volume It acts on the kidneys to cause small increase in GFR and decrease in sodium reabsorption