ArticleBritish journal of pharmacology2005
Deoxycholic acid inhibits pacemaker currents by activating ATP-dependent K+ channels through prostaglandin E2 in interstitial cells of Cajal from the murine small intestine.
Article in British journal of pharmacology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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13 citing papers in PubMed, 32 citations in OpenAlex.
- Ursodeoxycholic acid improves gastrointestinal motility defects in gallstone patients.World journal of gastroenterology · 2006Trial
- Review
- Differential responses to prostaglandins in the circular and longitudinal muscle layers of the murine ileum.American journal of physiology. Gastrointestinal and liver physiology · 2025Article
- Riboflavin metabolism involved into comparison of therapeutic action of wild-simulated and transplantedChinese herbal medicines · 2025Article
- The Mechanism of Action of Ghrelin and Motilin in the Pacemaker Potentials of Interstitial Cells of Cajal from the Murine Small Intestine.Molecules and cells · 2019Article
- Pituitary Adenylate Cyclase-activating Polypeptide Inhibits Pacemaker Activity of Colonic Interstitial Cells of Cajal.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2015Article
- Effects of ginsenoside on pacemaker potentials of cultured interstitial cells of Cajal clusters from the small intestine of mice.Molecules and cells · 2012Article
- Bile Acid Inhibition of N-type Calcium Channel Currents from Sympathetic Ganglion Neurons.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2012Article
- Interplay of hydrogen sulfide and nitric oxide on the pacemaker activity of interstitial cells of cajal from mouse small intestine.Chonnam medical journal · 2011Article
- Hydrophobic bile salts inhibit gallbladder smooth muscle function via stimulation of GPBAR1 receptors and activation of KATP channels.The Journal of physiology · 2010Article
- Receptor tyrosine and MAP kinase are involved in effects of H(2)O(2) on interstitial cells of Cajal in murine intestine.Journal of cellular and molecular medicine · 2010Article
- Inhibition of pacemaker currents by nitric oxide via activation of ATP-sensitive K+ channels in cultured interstitial cells of Cajal from the mouse small intestine.Naunyn-Schmiedeberg's archives of pharmacology · 2007Article
- Calcium-associated mechanisms in gut pacemaker activity.Journal of cellular and molecular medicineReview
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Authors and funding
9 authors at 3 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
1. We investigated the role of deoxycholic acid in pacemaker currents using whole-cell patch-clamp techniques at 30 degrees C in cultured interstitial cells of Cajal (ICC) from murine small intestine. 2. The treatment of ICC with deoxycholic acid resulted in a decrease in the frequency and amplitude of pacemaker currents and increases in resting outward currents. Also, under current clamping, deoxycholic acid produced the hyperpolarization of membrane potential and decreased the amplitude of the pacemaker potentials. 3. These observed effects of deoxycholic acid on pacemaker currents and pacemaker potentials were completely suppressed by glibenclamide, an ATP-sensitive K(+) channel blocker. 4. NS-398, a specific cyclooxygenase-2 (COX-2) inhibitor, significantly inhibited the deoxycholic acid-induced effects. The treatment with prostaglandin E(2) (PGE(2)) led to a decrease in the amplitude and frequency of pacemaker currents and to an increase in resting outward currents, and these observed effects of PGE(2) were blocked by glibenclamide. 5. We next examined the role of deoxycholic acid in the production of PGE(2) in ICC, and found that deoxycholic acid increased PGE(2) production through the induction of COX-2 enzyme activity and its gene expression. 6. The results suggest that deoxycholic acid inhibits the pacemaker currents of ICC by activating ATP-sensitive K(+) channels through the production of PGE(2).
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