Human intestinal potential difference: recording method and biophysical implications.

Gustke, Robert F.; McCormick, Patrick N.; Ruppin, H; Soergel, Konrad H.; Whalen, George E.; Wood, Carol M.

doi:10.1113/jphysiol.1981.sp014003

Cited by 21 publications

(16 citation statements)

References 29 publications

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“…These concentrations of ethanol could adversely affect the epithelial layer of the gastric mucosa and thereby reduce PD. Indeed, the present findings are in agreement with other studies [10,11] that the mucosal epithelial cells represent an important layer which generates PD, because neither acid secretion nor microscopic appearance of the oxyntiTaMe 1 Effects of mucosal exposure to ethanol (from 15 to 60 rain) on transmucosaI potential difference (PD), electrical current (I) and resistance (R). Values indicate means _+ SEM of 6 preparations.…”

Section: Discussionsupporting

confidence: 94%

In vitro study of ethanol on the electrical parameters in rat stomachs

Cho

1991

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The electrophysiological effects of mucosal or submucosal ethanol (5, 10, or 20%) were assessed in isolated stomach preparation. Mucosal incubation with these concentrations of ethanol dose- and time-dependently decreased the transmucosal potential difference (PD), while the electrical current (I) and resistance (R) were unaffected. Submucosal exposure to the same concentrations of ethanol also reduced the PD, but to a lesser extent; only 20% of ethanol produced a significant effect. This same dose of ethanol not only decreased I but also increased R to a significant level. These findings indicate that transmucosal PD appears to be generated largely by the mucosal epithelial cell barrier, while the I and R are elicited by the laminea propria mucosa which is easily approached and altered by ethanol which acts from the submucosal side. The significance of the effects produced by mucosal or submucosal ethanol is discussed.

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Section: Discussionsupporting

confidence: 94%

In vitro study of ethanol on the electrical parameters in rat stomachs

Cho

1991

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“…Normally, the paracellular channels in the small intestine intrinsically favored positively charged molecules and ions, i.e., high P Na /P Cl ratio (24,57), as confirmed by P Na /P Cl of 2.4 and 3.7 in the duodenum and Caco-2 monolayer, respectively. After a direct exposure to PRL, P Na /P Cl in both duodenal tissue and Caco-2 monolayer was elevated due to an increase in P Na in both cell types.…”

Section: Discussionmentioning

confidence: 99%

Prolactin-stimulated transepithelial calcium transport in duodenum and Caco-2 monolayer are mediated by the phosphoinositide 3-kinase pathway

Jantarajit¹,

Thongon²,

Pandaranandaka³

et al. 2007

American Journal of Physiology-Endocrinology and Metabolism

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Jantarajit W, Thongon N, Pandaranandaka J, Teerapornpuntakit J, Krishnamra N, Charoenphandhu N. Prolactin-stimulated transepithelial calcium transport in duodenum and Caco-2 monolayer are mediated by the phosphoinositide 3-kinase pathway. Am J Physiol Endocrinol Metab 293: E372-E384, 2007. First published May 8, 2007; doi:10.1152/ajpendo.00142.2007 has been shown to stimulate intestinal calcium absorption but the mechanism was still unknown. This study aimed to investigate the mechanism and signaling pathway by which PRL enhanced calcium transport in the rat duodenum and Caco-2 monolayer. Both epithelia strongly expressed mRNAs and proteins of PRL receptors. Ussing chamber technique showed that the duodenal active calcium fluxes were increased by PRL in a dose-response manner with the maximal effective dose of 800 ng/ml. This response diminished after exposure to LY-294002, a phosphoinositide 3-kinase (PI3K) inhibitor. Caco-2 monolayer gave similar response to PRL with the maximal effective dose of 600 ng/ml. By nullifying the transepithelial potential difference, we showed that the voltage-dependent paracellular calcium transport did not contribute to the PRL-enhanced flux in Caco-2 monolayer. In contrast, the calcium gradient-dependent paracellular transport and calcium permeability were increased by PRL. Effects of PRL on Caco-2 monolayer were abolished by PI3K inhibitors (LY-294002 and wortmannin), but not by inhibitors of MEK (U-0126) or JAK2 (AG-490). To investigate whether the PRL-enhanced paracellular transport was linked to changes in the epithelial charge selectivity, the permeability ratio of sodium and chloride (P Na/PCl) was determined. We found that PRL elevated the P Na/PCl in both epithelia, and the effects were blocked by PI3K inhibitors. In conclusion, PRL directly and rapidly stimulated the active and passive calcium transport in the rat duodenum and Caco-2 monolayer via the nongenomic PI3K-signaling pathway. This PRL-enhanced paracellular calcium transport could have resulted from altered charge selectivity. charge selectivity; dilution potential; paracellular transport; prolactin receptor; tight junction; transcellular transport AS ONE OF THE CALCIUM-REGULATING HORMONES during pregnancy and lactation, prolactin (PRL) has been shown to stimulate intestinal calcium absorption (38), thereby protecting against development of negative calcium balance during these reproductive periods. Further investigations in nonmated female rats also revealed stimulatory actions of PRL on intestinal calcium absorption (11, 54), especially in the duodenum which was the most efficient site for calcium transport (21,32). Although the presence of PRL receptor (PRLR) proteins in duodenal enterocytes of rats was controversial, expression of rat PRLR (rPRLR) transcripts in the duodenal mucosa, demonstrated by in situ hybridization technique (45), implicated a direct action of PRL on the duodenal epithelial cells.Calcium traversed the duodenal epithelium by both active and passive pathways with the former being neglig...

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“…It is likely that the paracellular pathway of both human jejunum and ileum are cation selective on the basis of measurements of dilution potentials elicited in vivo by nonelectrolytes (24,25); but, an extended experimental analysis of human small intestine does not yet exist. Many studies have used the Caco-2 cell system as an in vitro model for human small intestinal permeation (e.g.…”

Section: Introductionmentioning

confidence: 98%