Renal regulation of ECF potassium Flashcards
3 rules for potassium regulation
1) all filtered K+ is obligatorily reabsorbed so regulated K+ secretion in fine tuning segments determines K+ excretion and ECF potassium balance
2) variable secretion of K+ accounts for homeostasis
E = F - R + S
E = S because what is filtered is reabsorbed (prox tubule and loop)
bulk of filtered K+ (80%) reabsorbed in __
reabsorption of K+ is ___ and ___ driven by the ___
because it is freely permeable in tight junctions, it is swept along with ___ movement to the ___ side of the epithelium
1) proximal tubule
2) paracellular and passive; driven by the bulk flow of water through the tight junctions
3) water movement to the serosal side of epithelium
drives Na+ into serosal, Cl- follows and water follows through tight junction that sweeps along K+
1) in the loop of henle, K+ movement is largely ___, first using the ___ cotransporter at the apical membrane to gain access in a ___ transport process
2) K+ runs down its ____ through a ___ to the serosal/basolateral side
3) loop of henle accounts for ___ % of filtered load reabsorption
1) transcellular using Na/K/2Cl; gain access in secondary active transport process
2) electrochemical gradient through a K+ channel
3) 10-15%
secretion of K+ occurs in the ___ of the fine tuning segments (distal tubule/collecting duct)
principal cells (single cilia)
Secretory process has two parts
opposite of ___ transport
1) basolateral entry of K+ into cell via Na/K atpase
2) apical secretion of K+ into the tubular lumen
coupled to Na+ transport (in aldosterone sensitive cells)
______
reverse Na+ transport
balanced by charge neutrality from Na+ movement in opposite direction
2 steps in secretion
1) Na/K atpase to pump K across basolateral membrane into cell (Na out, K in)
2) K+ ion flow passively along electrochem gradient through K+ channel in apical membrane into lumen
3) excreted in urine
Feedback mechanism of incr K+ ingestion
mass action route
1) incr K+ ingestion
2) incr K+ in ECF
3) incr basolateral pumping of K+ into cell (MASS ACTION)
4) incr intracellular K+
5) incr driving force for apical K+ movement into lumen (urine)
6) incr K+ secretion and excretion
feedback mechanism of incr K+ ingestion
hormonal route (aldosterone in adrenal cortex)
1) incr K+ ingestion into ECF
2) incr stim of adrenal cortex cells
3) incr aldosterone syntehsis
4) incr # Na/K atpase in basolateral and incr in apical Na+ and K+ channels
5) incr basolateral pumping of K+ into cell and MASS ACTION ROUTE
incr permeability of lumenal membrane to K+
6) incr K+ secretion and excretion
What is the flow effect on K+ movement
drives passive movement of K+ through potassium channels from cell to lumen (incr permeability of lumenal membrane and incr driving force into lumen)
if you have slow tubular flow, how does that affect movement of K+
movement of K+ into lumen is slowed
more time for K+ to build up in tubular fluid before washed away by flow downstream
as lumenal K+ builds up, electrochem gradient for secretion decr (because close to electromchem equilibrium for K+)
secretion decr
if you have incr tubular flow what happens to K+ mvoement
K+ will better wash away newly secreted K+ before it builds up
keeps electrochem gradient high
K+ secreted is washed away by fast tubular flow so secretion rate remains elevated
what happens with loop diuretic on tubular flow
1) block Na/K/2Cl
2) inhibit NaCl excretion, inhibit H2O reabsorption
3) incr tubular flow because more H2O stays in tubule
4) incr K+ secretion and incr K+ excretion –> K+ wasting
also diuretic incr K+ excretion to 150% rate (10x faster rate of excretion than just inhib Na/K/2Cl due to incr tubular flow)
2) 25% NaCl in asecending limb drives out water from descending limb and distal tubule/collecting duct (ADH area) keeping interstitium hypertonic
How does K+ movement change if you applied lasix
block Na/2Cl/K transporter in descending limb of loop of henle
decr hypertonicity of interstitim (less Na/K/Cl move out)
less water reabosrbed
incr tubular flow
incr K+ excretion
how does alkalsosis affect K+ level and secretion
alkalosis –> hypokalemia
1) incr ECF pH (decr [H+]; as H+ leave, induce K+ to enter
loss of H+ from cells due to lower driving force for H+ into cells –> (H+ normally block Na+ channel) –> incr K+ permeability of apical K+ channels for K+ excretion
2) shift K+ from ECF into all cells
3) incr driving force for apical secretion and excretion
incr passive entry of K+ into principal cells
incr gradient for K+ excretion in Step 2 (across lumen) –> incr K+ excretion (hypokalemia)
4) decr K+ in ECF (hypokalemia)
5) also incr permeability of K+ in distal tubule and collecting duct on apical, incr K+ secretion
how does incr ECF pH affect K+ level
1) shift of K+ into cells
2) decr K+ concentration of ECF –> hypokalemia
incr K+ channel permeability because less H+ inhib apical K+ channels –> incr K+ secretion
3) incr intracellular K+
4) incr driving force for apical K+ secretion into lumen (incr permeability)
5) incr K+ secretion and excretion beyond needed for ECF balance–> hypokalemia