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Questions and Answers:
UF IDP Program: Molecular Aspects of Acid-Base Transport
Provided by:
I. David Weiner, M.D.
Professor of Medicine and Physiology
University of Florida College of Medicine and NF/SGVHS
Please e-mail me, at weineid@ufl.edu,
with your questions.
If you'd like to meet with me, either individually or as a group, please call
me at 374-6102 to arrange an appointment.
Dr. Weiner,
I had a couple questions about last week's lecture you gave.
1. During proximal tubule HCO3 reabsorption, you mentioned that via NCB1, three
HCO3 go into the blood for every Na+ and this results in a net charge of -2.
What is the effect of this imbalance on the blood??
- I didn't mention all of the ion transport that occurs, as it gets very
complicated. Basically, there are also chloride channels present in
the basolateral plasma membrane, that enable Cl- transport that
counterbalances the charge moved by NBC1.
2. In HCO3 reabsorption in the collecting duct I noticed that H2CO3
does not utilize a carbonic anhydrase to catalyze the reaction H2CO3 -> H2O +
CO2. Why is this? I have written that the flow rate in the collecting duct is
slower... is that the flow rate of H2CO3 into the blood due to a missing
carbonic anhydrase?
- The lack of luminal carbonic anhydrase (CA IV) is very important to
maximize ammonia secretion. In the absence of luminal CA IV, protons
secreted by either H-ATPase or H-K-ATPase are not immediately buffered by
luminal bicarbonate. As a result, Henderson-Hassellbach equation (H+ +
HCO3- <--> H2CO3 <--> H20 + CO2) is not in equilibrium, and luminal proton
concentration is higher than otherwise predicted. This is termed a
"luminal disequilibrium pH." This 'additional luminal acidification'
enable a rate of luminal ammonia secretion greater than would otherwise be
predicted. Thus, the benefit is a faster rate of ammonia secretion.
3. Regarding the ammonia transporters, in general does RhBG take ammonia out of
luminal fluid and into the cells and RhCG takes ammonia out of the cells and
into the blood?
- That appears to be the case.
4. In a slide titled Role of Rh Glycoproteins in renal ammonia transport
there is a diagram showing movement of NH3 through a cell using Rh
glycoproteins. It appears as though there is no net movement of NH3 in this
diagram. Both NH3 AND NH4 seem to be
moving in both directions in and out of the cell.
- Actually, NH3 enters across the basolateral membrane and is secreted
into the luminal fluid across the apical membrane.
- This vectorial transport appears to be due to net concentration
gradients for NH3, NH4+ and protons. Both RhBG and RhCG appear capable
of bidirectional transport.
5. Finally, you said that the effect of chronic metabolic acidosis on
urinary ammonia excretion was a 30 fold increase. Why is ammonia being excreted
if it is needed to buffer the acidosis???
- The ammonia excretion buffers the acidosis by enabling protons to be
secreted into the urine and excreted without substantially altering urine
pH.
Sorry for the abundance of questions.
thank you,
- Not a problem - I hope this helps.
I. David Weiner, M.D.
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