Test2: Wk7: 3 Renal tubular acidification - Puri Flashcards
kidneys filter — mmol bicarb / day
4320mmol
— mmol H+ neutralized by bicarb / day
70mmol
the kidneys filter — mmol of bicarb and generate — mmol of new bicarb
4230mmol and 70mmol
sodium hydrogen exchanger (NHE) transports H+ in the — and —
PT and TAL
H+ primary transporter
HATPase
Secondary H+ transporter
HK exchanger - only used with K deficit
H+ secretory system is located in
alpha intercalated discs in cortical collecting tubule/ duct
hyper aldosterone leads tp
metabolic alkylosis
aldosterone has 3 effects
- directly stimulate H-ATPase
- ⬆ Na-K-ATPase which ⬆ Na gradient to enter cell
- ⬆ ENaC activity and number which ⬆ luminal negativity secreting more H+
Bicarb Secretory system is located
beta intercalated cells in the cortical collecting tubule/ Duct
Bicarb Secretory system is only used during
metabolic alkylosis
beta intercalated cells secrete — into the lumen in exchange —
bicarb, Cl-
the proximal tubule and the TAL secrete H+ to
reclaim all bicarb
The — mediates most of HCO3- absorption in the P.T.
The apical membrane Na/H anti-porter
The apical membrane Na/H anti-porter are inhibited by
lithium and amiloride.
The Na/H anti-porter is exquisitely sensitive to
H+ concentration on the inside (cytoplasmic side) of the vesicle.
— is the Na/H anti-porter subtype predominantly responsible
NHE3
NHE3 activity stimulated by (2) and inhibited by (2)
AngII and endothelin; inhibited by PTH and PKA.
The Second Step: Generation of “new bicarbonate” and EXCRETION of H+ needs
urinary buffers —phosphates and ammonia
Step 1
reabsorb all filtered bicarb
Whenever an H+ secreted into the tubular lumen combines with a buffer other than HCO3- the net effect is
addition of a new HCO3- to the blood
Metabolically-derived NH3 is the second (and more important)
proton acceptor in the tubular fluid
NHE in the proximal tubule and H+-ATPase in the distal tubular segments (intercalated cells) allow
H+ movement into the tubular lumen
Protonation of NH3 also leads to synthesis of
one new molecule of HCO3-
Combined titrable and non titrable (NH4+) acid secretion equals
the amount of new HCO3- synthesized by the kidneys
Net acid excretion should be
the same the amount of new bicarb created
NAE =
rate of NH4+ excretion + rate of titratable acid (T.A.) excretion minus rate of HCO3-excretion
For each NH4+ excreted, —- new HCO3- is added to renal venous blood
1
For each H+ excreted combined with HPO4- - ( = T.A.) — HCO3- is added to the renal venous blood.
1
bicarb is filtered at the
glomerulus
bicarb is consumed by — and generated —
H+; daily
why is H+ secreted
to reabsorb all HCO3-
HCO3- reabsorption conserves extracellular
buffer anion
HCO3- reabsorption is driven by
active H+ secretion
For each H+ secreted, — HCO3- is reabsorbed
1
In proximal tubule & thick ascending limb % of filtered HCO3- is reabsorbed
90%
In proximal tubule & thick ascending limb H+ secretion occurs mostly by
antiport with Na+
In proximal tubule & thick ascending limb Minimal urine pH is —
6.4
In proximal tubule & thick ascending limb Carbonic anhydrase acts at the — of — and in the — of —
luminal membrane (proximal tubule)
cytoplasm (proximal tubule and thick ascending limb)
In collecting duct intercalated cells — remaining HCO3- is reabsorbed
Almost all
In collecting duct intercalated cells Minimal urine pH is —
4.4
In collecting duct intercalated cells H+ secretion occurs by (2)
H+ ATPase & H+, K+ ATPase
In collecting duct intercalated cells Carbonic anhydrase acts
only in the cytoplasm
—, —, and — stimulate H+ secretion
and HCO3- reabsorption
Falling pH, cortisol and endothelin
Elevated PCO2 directly stimulates
H+ secretion
As acids consume HCO3- and generate H2CO3 and then CO2, this directly activated — cells to increase — activity
PT; NHE
By Causing Intracellular Acidosis, Hypokalemia Increases
NHE3 Activity
Hypokalemia promotes — in the distal nephron
H/K exchange
High Aldosterone Causes
Alkalosis
