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Published on: March 16, 2017
In vitro potassium transport in the mouse small intestine
Eiko Inagaki1, Koichi Kawamata, Yuichi Suzuki
1Laboratory of Physiology, School of Food and Nutritional Sciences, University of Shizuoka, Shizuoka, 422-8526 Japan. e-ina@nuas.ac.jp
Insights
Potassium (K+) absorption in the small intestine involves more than just passive diffusion. Active transport mechanisms and cellular pathways also contribute to K+ uptake, with potential regulation by cAMP and aldosterone.
Area of Science:
- Gastroenterology
- Physiology
- Molecular Biology
Background:
- Potassium (K+) absorption in the small intestine is traditionally attributed to passive paracellular diffusion.
- The precise mechanisms and regulatory factors governing intestinal K+ absorption require further elucidation.
Purpose of the Study:
- To investigate the mechanisms of K+ absorption in the mouse ileum.
- To determine the contribution of passive and active transport pathways to K+ uptake.
- To explore the role of cAMP and aldosterone in regulating intestinal K+ transport.
Main Methods:
- Utilized in vitro Ussing chamber techniques with Rb+ (a K+ analog) flux measurements in mouse ileum.
- Employed atomic absorption spectroscopy to quantify unidirectional Rb+ fluxes (J(ms) and J(sm)).
- Assessed the impact of transmucosal potential (V(t)) changes, forskolin treatment, and low-sodium diet on Rb+ transport.
Main Results:
- Demonstrated net mucosal-to-serosal Rb+ absorption (J(net) > 0), indicating net K+ uptake.
- Identified both V(t)-dependent (diffusion) and V(t)-independent (non-diffusion) components in mucosal-to-serosal flux.
- Showed that forskolin and a low-sodium diet increased serosal-to-mucosal flux (J(sm)), thereby reducing net absorption.
Conclusions:
- Intestinal K+ absorption occurs via both passive paracellular diffusion and an active cellular transport mechanism.
- Cyclic adenosine monophosphate (cAMP) and aldosterone may play regulatory roles in intestinal K+ transport.
- These findings challenge the sole reliance on passive diffusion models for K+ absorption in the small intestine.
Abstract:
Ingested K+ is believed to be absorbed mainly in the small intestine by passive diffusion through the paracellular pathway. To further clarify K+ absorption in the small intestine, we determined the unidirectional flux values of Rb+ in vitro by atomic absorption spectroscopy in the mouse ileum mounted in Ussing chambers under short-circuit conditions. The mucosal-to-serosal Rb+ flux (J(ms)) was larger than the serosal-to-mucosal Rb+ flux (J(sm)), resulting in positive net Rb+ absorption (J(net)). The effect of changing the transmucosal potential (V(t)) showed that J(ms) was composed of both a V(t)-dependent diffusion component and a V(t)-independent non-diffusion component, while J(sm) was composed mainly of a V(t)-dependent component. A forskolin treatment eliminated J(net) mainly due to the increase in J(sm). When animals were fed a low-Na diet, J(net) was mainly eliminated as a result of the increase in J(sm). These findings suggest that K+ is absorbed not only by passive diffusion through the paracellular pathway, but also by an active transport mechanism operating through the cellular pathway. In addition, cAMP and aldosterone may be involved in regulating intestinal K+ transport.
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