Renal- Regulation of Electrolytes - Lecture 9 Flashcards
Why is the regulation of K+ within narrow limit so crucial to life?
- Regulates Cell volume
- Intracellular pH
- Synthesis of DNA and protein
- RMP
- Cardiac and neuromuscular activity
Describe the following in terms of intake & output:
- Positive K balance
- Negative balance
Which is hyperkalemia & which is hypokalemia?
- Positive K: intake > output (hyperkalemia)
2. Negative K: intake < output (hypokalemia)
An change in which hormones stimulates the movement of K INTO cells and decreases plasma volumes?
Does the concentration of the hormones have to increase or decrease for the aforementioned changes to occur?
- Insulin
- Epinephrine
- Aldosterone
- all have to increase; stimulate K moving into the cell (via na/k ATPase for example)
When is an individual in K balance? What is K excretion regulated by? (3)
When K intake = K output (plus output by the gastrointestinal tract)
- K excretion is regulated by
1. ADH
2. Aldosterone
3. Plasma K
What are 3 mechanisms in which K+ is released from cells ?
Briefly describe how these changes occur.
- Epinephrine - exercise & alpha 1 receptor stimulation causes K+ to be released (action potentials) –> vasoconstriction
- Cell Lysis (surgery, burns)
- Hyperosmolality
- cells shrink, K concentration inside the cell increases, this increases the driving force on K to LEAVE the cell
What are 5 mechanisms in which K is taken UP INTO THE CELL?
- Na/K ATPase
- increase in extracellular K stimulates Na/K ATPase uptake of K into cells - Insulin
- shifts K into cells post prandial - Epinephrine
- stimulation of B2 receptors - Aldosterone
- stimulation of Na/K ATPase
- increased urinary excretion of K - HYPOSMOLALITY
- cells swell–> [K] inside the cell is diluted –> increases the driving force of moving K INSIDE the cell
What is the normal excretion & reabsorption of K+ by the kidney?
How do these values changed with increased/decreased dietary K+ intake?
Excretion - 15%
Reabsorption - 85%
Increase dietary K: enhanced K+ EXCRETION (to 80%)
Decrease Dietary K: enhanced K+ REABSORPTION (to 99%)
What are the 3 principal factors that regulate the rate of K+ secretion by DT and CD?
- Na/K ATPase pump
- tubular cell to tubular lumen electrochemical gradient (-40mV)
- K+ permeability of apical membrane
Describe the mechanism of increased K outside the cell & aldosterone in regulating K+ secretion.
- Increased [K+] outside–> stimulates Na/K -ATPase –> increases [K]inside –> increases apical membrane permeability to K+ –> increases K+ secretion
- Increased [K+] outside –> stimulates aldosterone –> stimulates K+ secretion
In response to potassium depletion, which parts of the nephron decrease their secretion of K+? How much of the filtered load of K+ is excreted under these conditions?
How much is excreted under normal/high K+ conditions?
- Distal Tubule
- Cortical Collecting Duct
- Medullary Collecting Duct
1% under low K+
15%-85% under normal/high K+
What hormones alter K+ secreting?
- Aldosterone –> stimulate Na/K ATPase (increase K inside the cell) –> Increase K secretion
- Glucocorticoids –> increase K+ secretion (indirect via GFR increases!)
ADH has an affect on K+ secretion. True or false.
FALSE no net affect on K+
What 3 factors alter K+ secretion?
- Hormones (Aldosterone & Glucorticoids)
- Tubular Flow Rate –> increase flow = increased secretion
- Dietary Intake –> high K+ diet = high secretion
If distal tubule flow rate increases (diuresis) how is K+ secretion & ADH changed?
Increased flow rate results in increased K+ secretion and decreased ADH
- this results in tubular negativity
- which finally results in decreased K+ secretion (or K+ balance maintained)
If one’s diet is low in K+, how is secretion and excretion of K+ changed?
Decreased K+ secretion & excretion (K+conservation)
- if you increase K+ diet = “K+ spilling”
What are the reasons that ADH has no affect on K+ secretion?
Increased ADH results in:
- Increased electrochemical for K+ across apical membrane
- Increase permeability of K+ on apical membrane
BUT!! It is opposed by the DECREASED FLOW RATE that results from an increase in ADH!
therefore the net K+ secretion is not affected by ADH!
How does ACUTE metabolic ACIDOSIS affect K+ secretion & excretion? Why?
- Decreases K+ permeability of apical membrane in DT and CD
this results in decreased K+ secretion and excretion!!!
A) inhibits Na/K ATPase pumps which results in increased plasma K and cells do not secrete the excess plasma K into the tubule since the increased H+ concentration also affects the pumps on the lumenal membrane
B) Decreases K+ permeability
How does CHRONIC metabolic acidosis affect K+ excretion and secretion?
Increased [K+ out/H+ in ] exchange –> this increases plasma K+
- increases in K+ plasma concentration activates aldosterone system
- increased K+ permeability of apical membrane in DT and CD
- increased secretion and excretion!!!
How do diuretics affect K+:
Which are K+ sparing and which are K+ wasting?
- Furosemide
- Acetazolamide
- Mannitol
- Spironolactone
- Amiloride
K+ Wasting: (FAM)
- Furosemide
- Acetazolamide
- Mannitol
K+ SPARING: (SAT)
- Spironolactone
- Amiloride
- Triamterene
Where is most calcium stored?
How much is in ICF? ECF?
How does acidosis affect free ionized Calcium concentration?
Alkalosis?
Calcium stored in bone –> 99%
ICF –> 1%
ECF –> 0.1%
Acidosis –> increased ionized Calcium = HYPERCALCEMIA
Alkalosis –> decreased ionized Calcium –> Hypocalcemia
ex: hyperventilation: results in respiratory alkalosis & decreases free Ca2+, thus the membrane is more excitable and people become irritated –> Hypocalcemia!!
What is the affect of PTH on calcium? How does this change Calcium excreted/reabsorbed in the kidneys? In bone?
PTH –> protects against low Ca2+
- senses low Calcium and increases reabsorption of Calcium by kidneys and increases bone resorption (breakdown) and increases CALCITROL which INCREASE FREE CALCIUM
How do the following affect Calcium:
- PTH
- Calcitrol
- Calcitonin
- PTH –> prevents low Calcium by increasing reabsorption in kidney and resorption in bone marrow
- Calcitrol –> prevents low Calcium by increasing calcium resorption from bone & decreasing calcium excretion
- Calcitonin –> prevents HIGH CALCIUM: increases calcium deposition in bone & increases calcium excretion
What is the affect of Calcitrol on calcium? How does this change Calcium excreted/reabsorbed in the kidneys? In bone?
- Calcitrol protects against low Ca2+
- senses decreased calcium or [HPO4]2- or [H2PO4]-
- Proximal tubule produces CALCITROL
- caclium resorption from bone and decreased calcium excretion
- increased [Ca2+]
Where is Calcitrol released from in the nephron?
Proximal Tubule!
What is the affect of CALCITONIN on calcium? How does this change Calcium excreted/reabsorbed in the kidneys? In bone?
Calcitonin (felon :)) protects against HIGH CALCIUM
- senses increased calcium
- increased Calcitonin
- Increased [Ca2+] deposition in bone
- Decreased [Ca2+] and increased Calcium excretion
= decreased [Ca2+]
How much of filtered calcium is reabsorbed in the nephron? What mechanisms facilitate the reabsorption of Calcium?
99%
- active & passive transport via transcellular and paracellular pathways
- Ca-ATPase and 3Na/Ca Antiporter
How is Calcium EXCRETION regulated?
Hromonally via PTH, Calcitrol, and Calcitonin
How does PTH affect plasma [phosphate] and excretion?
Increases plasma phosphate and excretion
- increases plasma calcium concentration via bone resorption
How does Calcitonin affect plasma [phosphate] and excretion?
decreases plasma [phosphate] and decreases excretion
- also DECREASES plasma Calcium (via deposition)
How does Calcitrol affect plasma [phosphate] and excretion?
increases plasma phosphate and DECREASES excretion
-also increases plasma Calcium via bone resorption
How does the kidney protect plasma [phosphate] from going too high aka the “spill-over” affect?
By keeping plasma [phosphate] very close to the RPT
- protects the plasma from high phosphate levels by regulating its excretion/reabsorption
How does alpha 1 receptor stimulation of epinephrine affect K+? B2?
alpha 1 = K+ OUT of cell –> action potential generated (vasoconstriction)
B2 = K+ INTO the cell –> vasodilation
State how the following affect Calcium & phosphate Excretion & plasma concentrations:
- PTH
- Calcitriol
- Calcitonin
- PTH:
a) increased [Ca2+] and [phosphate]
b) decreased Calcium excretion, increased phosphate excretion - Calcitriol:
a) increased [Ca2+] and [phosphate]
b) decreased Calcium excretion, DECREASED phosphate excretion - Calcitonin:
a) Decreased [Ca2+] and [phosphate]
b) increased Calcium excretion, and INCREASED phosphate excretion
