Potassium Balance

Question 1

body response to increase in serum K

Answer 1

uptake into cells via insulin and epinephrine for storage, followed by secretion by the kidney

Question 2

short term reservoir for K+

Answer 2

skeletal muscle- stim by aldo, epi,insulin via increased Na/K ATPase activity

Question 3

what is the hormonal response to higher K

Answer 3

acute increases cause insulin release from pancreas and aldo and epi release from adrenal gland, causing cellular uptake

Question 4

met alkalosis effect on K handling

Answer 4

H+ moves out of cell to raise serum pH, exchanged w/ K+ causing hypokalemia

Question 5

met acidosis effect on K handling

Answer 5

excess H+ move into cells in exchange for K moving out, hyperkalemia results

Question 6

segment responsible for K secretion

Answer 6

DCT and CD- principal cells and alpha intercalated responsive to aldo

Question 7

describe K reabsorption in PCT

Answer 7

solvent drag- follows water thru AQPs

Question 8

K reabsorption by thick ascending limb

Answer 8

depends on NKCC cotransporter, needs tubular K+ present

K+ is recycled back somewhat into lumen by apical ROMK, resulting positivity drives cations like Mg and Ca thru tight junctions

Question 9

describe K handling in the CCD

Answer 9

principal cells: secrete K via ROMK, dependent on lumen negativity generated by Na reabsorption from ENaC (aldo dependent)

alpha intercalated: rabsorb K from H/K ATPase antiporter (secretes H), upregulated when K+ falls

Question 10

list 5 stimulants of K secretion

Answer 10

1. plasma K increases- stimulate Na/K ATPase on basolateral (increases cellular K, higher gradient)
2. aldo: stimulates ENaC and Na/K ATPase and ROMK
3. dietary intake of K- increased ROMK
4. higher tubular flow rate- higher K gradient as lumen K is washed out past channels (as in osmotic diuresis)
5. tubular negativity

Question 11

2 inhibs of K secretion

Answer 11

ACE inhibs or ang blockers- decrease aldo, can cause hyperkalemia

tubular damage- can reduce K secretion