1. Role of Kidneys In Regulation Of Potassium Levels In ECF

2. 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

3. 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

4. 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

6. 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

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

9. Intercalated cells can reabsorb Potassium during Potassium depletion

10. 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

11. 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

12. (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

14. 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

15. 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

17. 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

18. 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

19. Role Of Kidneys In Regulation Of Calcium Levels In ECF

20. 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

21. 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

22. 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

23. 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

25. 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

26. 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

27. 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

28. 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

29. 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

31. 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

32. 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

33. 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

34. 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

35. 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

36. 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

37. 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