BIOL 2420 Lecture Notes - Lecture 12: Nephron, Proximal Tubule, Epithelium
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Unit 8 – Lecture 12
Kidneys Use Ammonia and Phosphate Buffers
- Kidneys take care of 25% of compensation that the lungs cannot handle
o Alter pH two ways
▪ Directly – excreting or reabsorbing H+
▪ Indirectly – changing the rate at which HCO3- buffer is reabsorbed or
excreted
- In acidosis
o Kidney secretes H+ into the tubule lumen, using direct or indirect active transport
o Ammonia from amino acids and phosphate ions in the kidney act as buffers,
trapping large amounts of H+ as NH4+ and H2PO4-
▪ Buffers allow more H+ to be excreted
▪ Phosphate ions are present in filtrate and combine with H+ secreted into
the nephron lumen
▪ Even with these buffers, urine can become quite acidic
• Down to pH 4.5
▪ While H+ is being excreted, the kidneys make new HCO3- from CO2 and
H2O
• HCO3- is reabsorbed into the blood to act as a buffer and increase
pH
- In alkalosis, the kidney reserves the general process just described for acidosis
o Excreting HCO3- and reabsorbing H+ in an effort to bring pH back into the normal
range
o Renal compensations are slower than respiratory compensations, their effect on
pH might not be noticed for 24-48 hours
o Once activated, renal compensations effectively handle all but severe acid-based
disturbances
- Cellular mechanisms for renal handling of H+ and HCO3- resemble transport processes in
other epithelia
o These mechanisms involve some novel membrane transporters
1. Apical Na+-H+ exchanger (NHE)
▪ An indirect active transporter that brings Na+ into the epithelial cell in
exchange for moving H+ against its concentration gradient into the lumen
▪ Plays a role in proximal tubule Na+ reabsorption
2. Basolateral Na+-HCO3- symporter
▪ Moves Na+ and HCO3- out of the epithelial cell and into the interstitial
fluid
▪ Indirect active transporter – couples the energy of HCO3- diffusing down
its concentration gradient to the uphill movement of Na+ from the cell to
the ECF
3. H+-ATPase
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Document Summary
Kidneys take care of 25% of compensation that the lungs cannot handle: alter ph two ways, directly excreting or reabsorbing h+ Indirectly changing the rate at which hco3- buffer is reabsorbed or excreted. H2o: hco3- is reabsorbed into the blood to act as a buffer and increase ph. The renal tubule (on top of these mechanisms) uses the ubiquitous na+-k+-atpase and the same hco3--cl- antiport protein that is responsible for the chloride shift in red blood cells. The proximal tubule excretes h+ and reabsorbs hco3- Most hco3- (cid:373)ust (cid:271)e rea(cid:271)sor(cid:271)ed to (cid:373)ai(cid:374)tai(cid:374) the (cid:271)ody"s (cid:271)uffer (cid:272)apa(cid:272)ity. Proximal tubule reabsorbs most filtered hco3- by indirect methods because there is no apical membrane transporter to bring hco3- into the tubule cell. Shows the way that bicarbonate is reabsorbed in the proximal tubule: h+ is secreted from the proximal tubule cell into the lumen in exchange for filtered.