Test 2: Wk7: 2 Tubular transport of K/Ca/Mg - Mangiarua Flashcards
Plasma K conc.
Range
4 meq/L
3.4-4.5 meq/L
fatal plasma K conc.
8 meq/L
Intracellular K conc.
145 meq/L
primary regulator of K
kidneys
K transport is
bidirectional
% K reabsorbed in proximal tubule
67%
% K reabsorbed in thick ascending limb
20%
% K remaining at start of distal convoluted tubule
13%
% of filtered K is reabsorbed prior to distal tubule regardless of dietary K
87%
K has a — reabsorption
net
proximal tubule K transport
active - pump on luminal and basolateral
passive - most reabsorption in PT is passive
Distal tubule and cortical collecting duct K transport
perform the fine-tuning of K+ excretion to
maintain K+ balance
a person on a low K+ diet, there is further reabsorption of K+ by the — of the late distal tubule and collecting ducts
α-intercalated cells
persons on a normal or high K+ diet, K+ is secreted by the — of the late distal tubule and collecting duct
principal cells
The principal cells, in the connecting tubule and cortical and medullary collecting duct, when stimulated by — will secrete —.
aldosterone
K+
— dominate the overall transport of K+ unless — is inhibited
Principal cells
Aldosterone
— secretion is increased by Na entrance through —
K; ENaC
sodium entrance through ENaC sodium channels causes (2)
- NA,K-ATPase stimulation
2. Depol of luminal membrane
Potassium entering via the Na,K-ATPase that is not secreted
recycles through basolateral channels.
amiloride inhibits
inhibits sodium entry, and therefore inhibits potassium
secretion
stimulates both sodium reabsorption and potassium secretion at multiple points.
Aldosterone
ROMK and BK Low K excretion
ROMK - sequestered
BK - closed
ROMK and BK Normal K excretion
ROMK - open
BK - Closed
ROMK and BK High K excretion
ROMK - open
BK - open
5 factors that alter K secretion
(1) Sodium Delivery to the Distal Nephron
(2) Aldosterone
(3) Plasma Potassium
(4) GI Hormones
(5) Angiotensin II
Sodium Delivery to the Distal Nephron on K secretion
High sodium delivery stimulates potassium secretion; low
sodium delivery inhibits it.
Aldosterone on K secretion
Increases Na-K-ATPase which supplies more potassium from the interstitium to the cytosol of the principal cells.
Stimulates the activity of ROMK channels in principal cell of the distal nephron
Plasma Potassium on K secretion
The Na-K-ATPase that takes up potassium in principal cells is highly sensitive to the potassium concentration
Plasma potassium concentration exerts an influence on potassium excretion but is not the dominant factor under normal conditions.
GI Hormones on K secretion
Gastrointestinal peptide hormones released in response to ingested potassium may be responsible for the response to dietary intake.
Angiotensin II on K secretion
Inhibitor of potassium secretion; decrease the activity of ROMK channels in principal cells.
Alkalosis results in — K from principal cells which leads to —
⬆ K secretion and depletion of K
elevated plasma pH is often associated with
hypokalemia.
Low plasma pH is often associated with
hyperkalemia
Total plasma calcium has 3 components
- 40% protein bound - no filter
- 50% ionized Ca and biologically active - filters
- 10% complexed with anions - filters
As the plasma H+ concentration increases, the concentration of ionized calcium —
increases
In acidosis, as more H+ are buffered by plasma proteins, bound calcium is
displaced from proteins causing plasma Ca to
increase
in alkalosis the release of H+ from plasma proteins causes the plasma
Ca to
decrease
% of filtered Ca reabsorbed
98-99%
PTH — Ca++ reabsorption in the kidney and increases [Ca++ ]ECF
increases
Ca paracellular reabsorption in proximal tubule
driven by solvent drag
Ca transcellular reabsorption in proximal tubule
uptake across the brush border via Ca permeable ion channel and exit across basolateral membrane via Ca ATPase
Ca reabsorption in thick ascending limb
paracellular - driven by the transepithelial electrochemical gradient
Ca reabsorption in distal tubule
transcellular
1 Ca enter through apical Ca ion channels
2 Ca binds calbindin and complex diffuses across the cell to deliver Ca to basolateral
3 Ca transported across basolateral by 3NaCa antiporter and Ca-ATPase
distal tubule is the site of Ca
Ca reabsorption regulation
— regulates calcium homeostasis
PTH
PTH action
increases plasma Ca conc.
PTH renal effects (3)
- promotes calcitriol formation
- increase Ca reabsorption
- increase phosphate excretion
PTH increases Ca++ reabsorption by: (2)
Increasing the transcription and open probability, and inhibition of endocytosis of the Ca++-permeable ion channel.
- Upregulating the expression of calbindin and NCX1.
% of plasma phosphate is unbound and — filtered
90%; freely
% of the filtered load of phosphate is —
90%; actively reabsorbed from the nephron
phosphate is Co-transported with Na+ across — driven by —
the luminal plasma membrane.
intracellular Na+ gradient.
Pi is reabsorbed via three sodium phosphate cotransporters
Npt2a, Npt2c and PiT-2.
sodium phosphate cotransporters, which are positioned in the — of —
apical membrane of renal proximal tubule cells
PTH inhibits reabsorption of phosphate in the
the proximal tubule
PTH stimulates the removal of — from the brush border of the —
NPT2; proximal tubule
% of plasma magnesium is protein bound
30% of plasma magnesium is protein bound ➞ non filterable.
% of plasma magnesium is ionized
60% of plasma magnesium is ionized ➞ filterable.
% of plasma magnesium is complexed to anions such as phosphate, citrate, and oxalate
10% of plasma magnesium is complexed to anions such as phosphate, citrate, and oxalate➞ filterable.
Mg reabsorption in proximal tubule is believed to be
paracellular aided by a chemical gradient generated by Na gradient
Mg reabsorption in Thick ascending limb
paracellular
Mg2+ reabsorption along the DCT, which is predominantly —
transcellular
Mg2+ entry across the DCT apical membrane may take place via the
TRPM6 cation channel; the key driving force is the inside-negative membrane potential.
