5. Regulation of K+ Balance

Question 1

How does strenuous exercise affect potassium balance?

Answer 1

Strenuous exercise enhances potassium efflux by increasing the presence of alpha-catecholamines.

Question 2

What is the function of aldosterone in potassium balance?

Answer 2

Renal: Increased potassium excretion by the kidney

Extrarenal: Increased potassium excretion through saliva and intestinal fluids.

Question 3

Overall, what do alpha-intercalated cells reabsorb/secrete?

Answer 3

Reabsorb: potassium: bicarbonate

Secrete: hydrogen ion and chloride

Question 4

What cell type reabsorbs potassium in the distal tubule?

Answer 4

Alpha-intercalated cells

Question 5

What is the function of alpha-catecholamines on potassium balance?

Answer 5

Alpha catecholamines decrease cell uptake of potassium by decreasing the activity of Na/K ATPase – by decreasing available cAMP.

Question 6

What are the two (listed) factors which stimulate potassium reabsorption?

Answer 6

Potassium deficiency (hypokalemia, or low potassium diet)

Potassium loss through severe diarrhea.

Question 7

What is the function of beta-catecholamines on potassium balance?

Answer 7

Beta catecholamines enhanced cell uptake of potassium by increasing the activity of the Na/K ATPase – by increasing available cAMP

Question 8

Overall, what do beta-intercalated cells reabsorb/secrete?

Answer 8

Reabsorb: hydrogen ion, chloride

Secrete: potassium, bicarbonate

Question 9

Overall, what do principal cells reabsorb/secrete?

Answer 9

Reabsorb: sodium, H2O

Secrete: potassium

Question 10

What is the basic mechanism for the effect of alkalosis on plasma potassium levels?

Answer 10

Alkalosis (increased pH) causes an increased activity in the Na/K ATPase of the distal tubule.

This results in a buildup of potassium inside the cells of the tubular lumen, which provides the concentration gradient for potassium to be secreted.

This causes hypokalemia.

Question 11

What are the six listed factors that stimulate potassium secretion?

Answer 11

Aldosterone.

Concentration of potassium in the extracellular fluid.

Increased tubular flow rates.

Stimulation of the Na/K ATPase.

Reduced back leakage of potassium (ICF through basolateral membrane).

Increase in synthesis of potassium channels inserted into the luminal membrane.

(All six increase potassium secretion)

Question 12

How do we ensure sodium makes it to the distal tubule to be available for significant potassium secretion if necessary?

Answer 12

Potassium is secreted by the inner and outer medullary collecting duct into the interstitial fluid where it stays until it is reabsorbed by the late proximal tubule / thin descending limb of the loop of Henle. This potassium field decreases the amount of sodium reabsorbed proximal to the distal tubule (specifically in the thick ascending limb by the Na/K/2Cl transporters), ensuring enough sodium is available for significant potassium reabsorption if necessary.

Question 13

How do alpha intercalated cells reabsorb potassium?

Answer 13

Carbonic anhydrase breaks down carbonic acid into hydrogen and bicarbonate. Bicarbonate is reabsorbed, and the hydrogen is excreted in exchange for a reabsorbed potassium.

Question 14

How do principal cells secrete potassium?

Answer 14

They reabsorb a sodium ion via the ENaC channel, and then exchange that sodium for a potassium ion which is secreted through Big Potassium, and Renal Outer Medullary Potassium channels.

Question 15

When we increase our sodium intake, aldosterone compensates.

What will be the effect of that compensation on potassium, and why doesn’t it make us hypo/hypokalemic?

Answer 15

When we increase sodium intake, aldosterone decreases to compensate.

This decrease in aldosterone increases reabsorption of potassium.

However, we don’t become hyperkalemic because the increase in sodium also increases the tubular flow rate in the distal tubule.
The increase in tubular flow rate washes out potassium and increases potassium secretion to balance the increased reabsorption.

Question 16

What is the effect of acute acidosis on potassium?

Answer 16

The increased acid inactivates the Na/K ATPase, decreasing the amount of sodium reabsorbed and the amount of potassium excreted.

This causes hyperkalemia.

Question 17

What is the effect of glucocorticoids and increased anion delivery on potassium secretion?

Answer 17

Glucocorticoids and increased anion delivery both increase potassium secretion by increasing fluid flow rate.

(The anions act as an osmotic diuretic – glucocorticoids directly increase GFR by binding to the same receptor as aldosterone)

Question 18

How do beta-intercalated cells secrete potassium?

Answer 18

Hydrogen is produced inside the cell by the action of carbonic anhydrase breaking down carbonic acid into hydrogen and bicarbonate (the latter of which is excreted). That hydrogen ion is then reabsorbed in exchange for a potassium ion, which is excreted.

Question 19

How would systemic alkalosis / acidosis affect plasma potassium levels?

Answer 19

Alkalosis would cause potassium to enter the cells in exchange for hydrogen, thereby creating hypokalemia (low plasma potassium)

Acidosis would cause potassium to exit the cells in exchange for hydrogen, thereby creating hyperkalemia (high plasma potassium)

Question 20

What is the function of epinephrine in potassium balance?

Answer 20

Epinephrine lowers serum potassium by encouraging uptake into extrarenal tissue cells.

Epinephrine’s alpha-1 receptors also encourage potassium excretion by the kidney, via stimulation of the Na/K ATPase – encouraging potassium to enter peritubular cells where potassium channels can secrete it into the urine.

Question 21

What is the function of insulin in potassium balance?

Answer 21

Insulin (like epinephrine) stimulates Na/K ATPase, causing potassium to enter the peritubular cells where it can then be ejected by potassium channels.

Question 22

Why might decreased flow rate decrease potassium secretion?

Answer 22

Decreased flow rate causes potassium to buildup in the intratubular fluid, which decreases the concentration gradient, making it harder to push potassium into the intratubular fluid.

Question 23

How is potassium reabsorbed by the proximal tubule?

Answer 23

Sodium is reabsorbed with bicarbonate leaving chloride behind, this creates a negative transepithelial potential difference. When chloride is reabsorbed paracellularly, this creates a positive transepithelial potential difference. That positive TEPD pushes potassium between the cells – paracellular reabsorption.

Question 24

Is hypokalemia typically associated with systemic acidosis, or alkalosis?

Answer 24

Hypokalemia is typically associated with systemic alkalosis.

(Aldosterone gets rid of potassium, and also causes alkalosis)

Question 25

What is the effect of chronic acidosis on potassium?

Answer 25

Chronic acidosis (unlike acute acidosis) increases potassium secretion.

(This is because prolonged inhibition of the Na/K ATPase decreases the reabsorption of water and solutes by the proximal tubule. This increases tubular flow to the distal tubule, therefore increasing potassium secretion. Also, the lack of water reabsorption stimulates the RAAS system, which produces aldosterone, which ejects potassium.)

Question 26

What would the effect of plasma hyperosmolality be on potassium balance?

Answer 26

Potassium rushes out of the intracellular space.

This is because water will leave the ICF, causing a net increase in potassium concentration in the ICF, causing a net pressure for potassium to leave.

Question 27

What two cell types in the distal tubule secrete potassium?

Answer 27

Principal cells

Beta-intercalated cells

Question 28

Why might increased flow rates increase potassium secretion?

Answer 28

Increased flow rate washes away potassium from the intratubular fluid, increasing the concentration gradient and making it easier to push potassium into the intratubular fluid.

Also, and increased flow rate increases the amount of sodium presented to the distal tubule. As that sodium is reabsorbed, there is a concomitant secretion of potassium.