8: Regulation of Potassium Balance

Question 1

Explain how K plasma cc is elevated after intense exercise or trauma and how it is quickly restored to normal (within minutes)

Answer 1

exercise –> rapidly firing action potentials –> K moves out of cells

trauma –> cell damage –> K released

both: norepinephrine release/sympathetic tone up –> NaKATPase upregulated

Question 2

What % of K is in the ECF?

Answer 2

2%

Question 3

How much of the filtered load of K is reabsorbed in the proximal tubules and loop of Henle? (give % for each)

Answer 3

65%, 25%

Question 4

How is K reabsorbed in the proxmal tubules?

Answer 4

by concentration gradient established through Na and water absorption

important: high NaKATPase activity as well –> must recycle this K back into the interstitium

Question 5

How is K reabsorbed in the loop of henle?

Answer 5

NaK2Cl pump

but, way less K than Na in tubular lumen –> for pump to work, K has to be recycled back into the lumen

Question 6

What is the name of the secretory potassium channels in the late distal tubules and principal cells of the connecting tubule and cortical collecting ducts?

Answer 6

ROMK (renal outer medulla K channel)

Question 7

What is the name of the secretory K channels that only function when high K excretion is required?

Answer 7

BK (“big capacity” K channel) - not open with normal K levels

Question 8

What are the 3 types of intercalated cells? which one regulates K excretion/reabsorption and how?

Answer 8

A, B and “non-A, non-B”

A participates in K homeostasis
* H-K-ATPase pump

Question 9

Summarize the activity of ROMK and BK channels under low K excretion, normal K excretion and high K excretion

Answer 9

Low K excretion:
* ROMK sequestered
* BK closed

normal K excretion:
* ROMK open
* BK closed

high K excretion
* ROMK open
* BK open

Question 10

How do the kidneys respond to a prolonged period of low K ingestion?

Answer 10

internalization of ROMK

Question 11

How does high tubular flow increase K secretion?

Answer 11

high flow –> removes secreted K –> keeps cc down and allows more secretion

BK becomes active under high flow

Question 12

Explain how hyperkalemia can increase K secretion through Aldosterone without affect Na absorption/secretion

Answer 12

hyperkalemia causes aldosterone release without causing ATII secretion

aldosterone –> increased NaKATPase and ROMK (but needs Na to work!)

ATII needed for NaCl channel activation by aldosterone
less NaCl channel absorption –> more Na for ENaC –> this upregulated Na absorption promotes more K secretion

Question 13

What is the effect on Angiotensin II on K secretion?

Answer 13

lowers K excretion

allows Na absorption with NaCl symporter, reduces ROMK acitivity

when ATII absent aldosterone –> inhibits NaCl symporter and stimulates ROMK and BK

Question 14

Describe what happens via the RAAS system in a patient with volume/Na depletion but normal K cc.

Answer 14

causes RAAS activation with ATII and aldosterone –> NaCl activation –> little Na left for ENaC channels –> less driving force for K secretion
ATII –> ROMK inhibition

Na absorption without excessive K loss

Question 15

Describe what happens via the RAAS system in a patient with hyperkalemia but normal ECF volume and Na.

Answer 15

hyperkalemia causes aldosterone release without causing ATII secretion

aldosterone –> increased NaKATPase and ROMK (but needs Na to work!)

ATII needed for NaCl channel activation by aldosterone
less NaCl channel absorption –> more Na for ENaC –> this upregulated Na absorption promotes more K absorption

Question 16

Describe what happens via the RAAS system in a patient with both hypokalemia and hyponatremia.

Answer 16

RAAS ativation –> ATII increases but aldosterone secretion is inhibited by low K

ATII upregulates NaCl symporter and downregulates ROMK

Question 17

How do diuretics cause K loss?

Answer 17

more Na delivered to the distal tubules and cortical collecting ducts –> more ENaC activity and therefore K secretion