Titratable acid excretion is an advanced renal phys topic...and this "pimp question" itself is pretty esoteric.
Potassium balance is best understood in relation to the collecting tubule. This is where the last 5% of K+ is handled and is most important in terms of Hyper/Hypokalemia. (Think of Hypokalemia in Hyperaldosteronism, the excess aldosterone acts solely at the level of the collecting tubule and is responsible for the low serum K+ levels). Further, distal Potassium handling is best understood in terms of distal H+ secretion, and therefore in terms of titratable acid excretion.
Nevertheless, there are 3 titratable, excreted acids and are best remembered in their base form [BECAUSE THIS IS HOW THEY ARE ACTIVELY TRANSPORTED ACROSS THE CELL MEMBRANE]:
1) Carbonic acid (remember as HCO3)
2) Ammonium (remember as NH3)
3) Phosphoric acid (remember as PO4)
Obviously, HCO3 titration is a proximal phenomenon. I will ignore the handling of HCO3 in the PCT as it is not pertinent in this situation since 2/3 of all K+ is reabsorbed here and is static regardless of physiologic plasma K+ levels. Furthermore, PO4 plays a much more minor role in urinary acidification and acid base titration and can, for the most part, be ignored when thinking of renal H+ excretion.
Remember in the collecting tubule, the
Intercalated Cell has a
K+/H+ exchanger in its lumenal membrane. This pump is prinicpally acitivated by:
increased intracellular [H+] --> avid K+ reabsorption into the tubular cell, increased H+ secretion into the lumen (and thus urinary excretion)
(
it is essential that you're able to distiguish lumenal vs.intracellular in order to understand renal solute handling)
Both Aldosterone and Hypokalemia result in ammoniagenesis, the mechanism is not completely elucidated. But, if you ascribe to Guyton's dogma, then you accept most titratable acid excretion occurs within the collecting tubule under the direction of the intercalated cell. This is a gross oversimplification, but it(urinary proton excretion) is easy to understand in this manner and will stand up to arguement.
If pimped, this would be my response: "Both Hypokalemia and Hyperaldosteronism are known to increase renal ammonia production in humans and animals, however the etiology is unclear{
FACT}. A possible explanation would be that by decreasing lumenal K+ there is less H+ exchange out of the tubular cell...therefore, intracellular <thus plasma> pH decreases{
ASSUMPTION}. Ammonia is produced to counteract the resultant "metabolic acidosis" via ammoniagenesis."
If you're unimpressed with my arguement, here is some further reading.
http://books.google.com/books?id=Dp...X&oi=book_result&resnum=6&ct=result#PPA209,M1
http://www.nature.com/ki/journal/v40/n4/pdf/ki1991274a.pdf
