Cited by 225Ion Transport and Channel RegulationRenal function and acid-base balanceDigestive system and related health

Mechanism of bicarbonate absorption and its relationship to sodium transport in the human jejunum

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Turnberg, Leslie A., Fordtran, John S., Carter, N. W., Rector, Floyd C.·1970·Journal of Clinical Investigation

Abstract

Using a constant perfusion technique, sodium and bicarbonate absorption was studied in human subjects. The following observations were made on sodium absorption from saline solution: (a) the rate of sodium absorption is markedly influenced by bulk water flow, (b) when net water flow is zero, sodium absorption is zero if there are no concentration gradients between plasma and lumen that favor net NaCl diffusion; and (c) the PD between abraded skin and jejunal lumen is near zero when saline is perfused and does not change with partial substitution of sulfate or bicarbonate for chloride. Based on these observations, we conclude that sodium absorption from saline is entirely passive in the human jejunum. On the other hand, in the presence of bicarbonate sodium is absorbed actively against electrochemical gradients. The mechanism of the link between bicarbonate and sodium absorption was studied in normal subjects and in 11 patients with pernicious anemia; the latter were chosen because they do not secrete gastric acid which can react with bicarbonate in the jejunal lumen. We observed that bicarbonate absorption (a) occurs against steep electrochemical gradients, (b) does not generate a potential difference between abraded skin and jejunal lumen, (c) is inhibited by acetazolamide, and (d) generates a high CO2 tension in jejunal fluid. These observations suggest that bicarbonate absorption is mediated by active hydrogen secretion, rather than by bicarbonate ion transport per se, and that the link between sodium and bicarbonate transport is best explained by a sodium-hydrogen exchange process.

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  • Bicarbonate anions are actively transported across the intestinal mucosa rather than passively and become saturated.

    “Bicarbonate anions are actively transported across the intestinal mucosa rather than passively and become saturated (Turnberg, 1970), which could explain why blood concentrations are reduced with enteric-coated NaHCO 3 .”

    From Enteric-Coated Sodium Bicarbonate Attenuates Gastrointestinal Side-Effects (2020) · cites this paper as Turnberg, 1970

    The Discussion says bicarbonate absorption is at least partially saturable at high luminal concentrations and can occur against steep electrochemical gradients. But the Introduction and Abstract attribute that absorption to active hydrogen-ion secretion, rather than direct transport of bicarbonate anions. Page numbers are not provided in our copy. (LLM, conf=0.90)

    Experimental — accuracy not yet measured
  • Bicarbonate ions are absorbed by an active ion transport process involving hydrogen ion secretion in the small intestine.

    “They are also absorbed by an active ion transport process involving hydrogen ion secretion in the small intestine [39,40].”
  • Since GI distress during sodium bicarbonate application may be partly attributable to degradation in the stomach, enteric coating can reduce the neutralizing effect of gastric acid and largely reduce side effects.

    “Since GI distress during sodium bicarbonate application may be partly attributable to degradation in the stomach (Turnberg et al., 1970), enteric coating can reduce the neutralizing effect of gastric acid and largely reduce side effects.”

    From Acute enteric-coated sodium bicarbonate has negligible effect on anaerobic performance but affects metabolomics and attenuates the gastrointestinal response (2022) · cites this paper as Turnberg et al., 1970

    The Methods section says the researchers avoided gastric-acid contamination of a jejunal perfusate; it does not discuss GI distress from oral sodium bicarbonate. Searches for stomach degradation, enteric coating, and side effects found no passage addressing the attributed claim. The cited paper therefore does not verify the proposed cause of GI distress. (LLM, conf=0.76)

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No references could be resolved yet.

Research works printed but not linked: 2

  1. Brodsky, W. A., and T. P. Schilb. 1967. Mechanism of acidification in turtle bladder. Fed. Proc. 26: 1314.
  2. Kennedy, T. J., Jr., M. Eden, and R. W. Berliner. 1957. Interpretation of urine C02 tension. Fed. Proc. 16: 72.

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Authors
Turnberg, L. A., Fordtran, J. S., Carter, N. W., & Rector, F. C.
Affiliations
The University of Texas Southwestern Medical Center (US)
Venue
Journal of Clinical Investigation
Published
1970-03-01
Volume
49
Issue
3
Pages
548-556
ISSN
0021-9738 (ISSN-L)
OpenAlex
W2169246244
Cited by
225
References
0
Citations by year
2026: 1 · 2025: 3 · 2024: 4 · 2023: 3 · 2022: 2 · 2021: 4 · 2020: 5 · 2019: 5 · 2018: 6 · 2017: 2 · 2016: 3 · 2015: 1 · 2012: 4
FWCI
4.31
Type
journal article
Language
en
Open access
Locations
  • Journal of Clinical Investigation (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion Transport and Channel Regulation
  • Health Sciences › Medicine › Nephrology › Renal function and acid-base balance
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Digestive system and related health
Keywords
bicarbonate uptake, sodium uptake, jejunum, Na+/H+ exchange, hydrogen ion secretion, pernicious anemia, acetazolamide, electrochemical gradient, intestinal epithelial transport, carbon dioxide tension
MeSH terms
Acetazolamide, Anemia, Pernicious, Bicarbonates, Biological Transport, Carbon Dioxide, Chlorides, Humans, Hydrogen, Hydrogen-Ion Concentration, Intestinal Absorption, Ion Exchange, Jejunum, Perfusion, Skin Absorption, Sodium, Water

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