Regulation of K Balance Flashcards
Role of Epinephrine in extrarenal regulation of plasma K+
Lowers serum K by uptake into cells of extrarenal tissues even while stimulating K+ excretion by kidney
differing responses for alpha and b receptor stimulation
Role of Insulin in extrarenal regulation of plasma K+
Stimulate Na/K ATPase causing flux of K+ into cells and efflux of Na+ from cellls
Insulin & Glucose administration can treat hyperkalemia
Role of Aldosterone in extrarenal regulation of plasma K+
- Renal
- Extrarenal
Renal: increase K+ excretion by kidney
Extrarenal: increase K+ secretion into intestinal fluids & saliva
Enhances acid excretion via production of systemic alkalosis (K is low)
Which factors enhance K+ uptake? how?
-Insulin and Beta- Catecholamines
both by activating Na/K ATPase (catecholamine is via cAMP)
- Alkalosis
“k is lo”
Which factors impairs K+ uptake? how?
-alpha catecholamines
opposite of beta
- acidosis
donnan effect; inhibit Na/K ATPase - Cell damage
release of intracellular contents
Which factors enhance K+ cell efflux? how?
-hyperosmolality
due to contraction of ICF volume and increased intracellular K+
- strenuous exercise
activating alpha catecholamines
Which factor has loose correlation/ effect on potassium?
external potassium balance
ration vs total body K+ until severe state
Filtered load equation
GFR * plasma concentration * % filterability
Plasma protein characteristics
- not filterable under normal circumstances
- any substance bound to plasma protein will not be filtered
PCT and PST
- what is always reabsorbed?
- what is mostly reabsorbed?
- what is secreted?
- major mechanism/ form of transport?
Always reabsorbed
- glucose
- amino acids
Most reabsorbed
- Na
- K
- Cl
- HCO3
- Ca
- P
Secreted
- cations and anions
- drugs, metabolites, creatinine, urate
Major mechanism
Na/K ATPase pump in basolateral membrane
K+ reabsorption in Proximal Tubule
- what does it effect
- locations
- similar to Na reabsorption
- does NOT play a direct role in regulation of K+ balance
- INDIRECT ROLE
- changing NaCl reabsorption has considerable effects on distal tubular flow and distal tubular Na+ delivery, which impacts K+ later on
PCT: S1 &S2
PST : S2 & S3
How does K+ get reabsorbed in PT? (8)
- driven by what?
1) Early PT, Na reabsorbed with HCO3
2) Cl gets let behind
3) Negative TEPD builds up
4) Cl is repelled and reabsorbed
5) Continued NaCL reabsorption drags water along (solvent drag)
6) Positive TEPD builds up as Cl- reabsorbs
7) Postive TEPD repels K
8) K reabsorbed paracellularly
driven by lumen-positive transepithelial potential difference (TEPD) - found in late proximal tubule
Early PCT reabsorbs a lot of sodium! Explain the effects of it?
Creates lumen-negative potential difference
pushes paracellular Cl- to get reabsorbed in the straight PT
reversal of the PD to a positive value will help push NA and K via paracellular reabsorption
Loop of Henle transport and medullary recycling steps (4)
1) K secreted in cortical CD
2) K reabsorbed by outer medulla CD and inner medulla CD
3) K+ floats in interstitium
4) K secreted into Late PT/descending thin limbs of LoH
Goal of Loop of Henle transport and medullary recycling
increase presence of medullary K
Purpose of Loop of Henle transport and medullary recycling
large K presence decreases NKCC2 reabsorption by TAL
-> enhanced Na-delivery to distal tubule-> stimulates NA reabsorption and K secretion-> helps you excrete K during dietary loading
Where is K+ secreted? reabsorbed?
BOTH in late DT and cortical CD
-according to needs of the body
What secretes K?
principal cells and beta-intercalated cells
Most important factors that stimulate potassium secretion
- by which channels
1) increased ECF (K)
2) aldosterone
3) increased tubular flow rate
potassium channels, epithelial sodium channels (EnaC), renal outer medullary potassium (ROMK)
What reabsorbs K?
alpha intercalated cells
Most important factors that stimulate potassium reabsoprtion
1) K deficiency, low K diet, hypokalemia
2) K loss through severe diarrhea
What is reabsorbed in these cells? What is secreted?
1) principal cells
2) alpha intercalated cells
3) beta intercalated cells
1) Principal cells
Reabsorbed: Na, H2O
Secretes: K
2) alpha intercalated cells
Reabsorbed: K+, HCO3
Secretes: H
3) beta intercalated cells
Reabsorbed: H, Cl
Secretes: K, HCO3
Factors that regulate K+ secretion (5)
Buildup of extracellular K
1) activate Na/K ATPase pump in basolateral membrane of principal cells
2) Reduced back-leakage of K+ from ICF to renal interstitium
3) activate synthesis of K channels and insertion into luminal membrane
4) activate aldosterone secretion
5) increased DT flow rate
How does increased flow rate enhance K secretion (2)?
dilutes K secreted in lumen -> increasing the K concentration gradient
Delivers more Na to DT for reabsorption-> gradient across the tubular cell rises-> K secretion is promoted
How does decreased flow rate slow K secretion
K concentrations build up earlier in the tubule-> decreasing concentration gradient between cell and tubular fluid-> secretion slows
Why is relationship between distal tubular flow rate and potassium secretion important? ( think aldosterone, sodium, potassium)
prevents physiological conflict between the role for aldosterone in regulation of potassium and sodium excretion
- increased flow rate in DT PRESERVE normal potassium excretion during changes in sodium intake and aldosterone levels
- high sodium/decreased aldosterone and high tubular flow rates counterbalance each other
Acute alkalosis
- effects
- acute process that decreases in H+ ion concentration in extracellular fluid
alkalemia ( high blood ph)
everything increases!! - increase Na/K atpase pump activity - increase k concentration - increase passive diffusion of K into tubule lumen - increase K channels - increase K secretion End result: hypokalemia ( K is lo)
Acute acidosis
- effects
- acute process that increases in H+ ion concentration in extracellular fluid
acidemia ( low blood ph)
everything decreases!! - decrease Na/K atpase pump activity - decrease k concentration - decrease passive diffusion of K into tubule lumen - decrease K channels - decrease K secretion End result: hyperkalemia ( K is lo)
Acute vs chronic acidosis
- elaborate on chronic acidosis ( 3)
TIME DEPENDENT
chronic acidosis stimulates K secretion
Chronic
1) decreases reabsorption of water and solutes in PT
- by inhibiting Na/K ATPase
2) increase tubular flow to DT and CD
3) RAAS stimulated bc of lack of water reabsorption and decrease of ECF volume
- Result: K secretion rises
Acidosis on stabilizing K secretion
acidosis-> decrease proximal reabsorption -> increase distal flow -> activate distal K secretion
acidosis -> decrease intracellular K content-> inhibit distal K secretion
Volume expansion on stabilizing K secretion
Volume expansion-> decrease proximal reabsorption -> increase distal flow -> activate distal K secretion
Volume expansion -> decrease aldosterone-> inhibit distal K secretion
High water intake (water diuresis) on stabilizing K secretion
high water intake-> decrease water reabsorption -> increase distal flow -> activate distal K secretion
high water intake -> decrease ADH-> inhibit distal K secretion
Volume Contraction on stabilizing K secretion
volume contraction-> decrease GFR -> decrease distal flow -> inhibit distal K secretion
volume contraction -> increase renin-> increase angiotensin II -> increase aldosterone -> activate distal K secretion
ADH on K+
increase K+ secretion
- via Na resorption and stimulation of K+ channels
Luminal flow rate on K+
increase K+ secretion
Acidosis on K+
decrease K+ secretion
Alkalosis on K+
increase K+ secretion
Glucocorticoids on K+
increase K secretion
- via binding of mineralocorticoid receptor
- increase GFR
- increase fluid flow rate
Anion delivery on K+
increase K secretion
- acts as osmotic diuretic
- increases tubular fluid flow rate
- impact electrochemical differences
What are some effect on Na Cl reabsorption in PT? (3)
- reduce Na+ delivery to the CNT and CCD
- decrease the lumen-negative potential
- decrease K + secretion
Aldosterone characteristics on K+
- akaliuretic hormone, induced by hyperkalemia
However, under certain circumstances associated with marked induction of aldosterone, such as dietary sodium restriction, sodium
balance is maintained without effects on K + homeostasis
- aldosterone-paradox
Effects of diuretics on K
inhibit Na reabsorption
- will promote K+
( exceptions are K sparing drugs)