Propofol inhibits carbachol-induced chloride secretion by directly targeting the basolateral K+ channel in rat ileum epithelium.

Tang, S-H; Wang, H-Y; Sun, H; An, Ning; Xiao, L; Sun, Q; Zhao, D-B

doi:10.1111/nmo.12934

Article (Scientific journals)

Propofol inhibits carbachol-induced chloride secretion by directly targeting the basolateral K+ channel in rat ileum epithelium.

Tang, S-H; Wang, H-Y; Sun, H et al.

2017 • In Neurogastroenterology and Motility, 29 (2), p. 12934

Peer Reviewed verified by ORBi

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https://hdl.handle.net/2268/291006

DOI
10.1111/nmo.12934

PubMed
27578144

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Keywords :

K+ channels; acetylcholine receptor; intestinal secretion; propofol; short-circuit current; Anesthetics, Intravenous; Chlorides; Potassium Channel Blockers; Potassium Channels; Carbachol; Propofol; Anesthetics, Intravenous/pharmacology; Animals; Carbachol/antagonists & inhibitors; Carbachol/pharmacology; Chlorides/antagonists & inhibitors; Chlorides/metabolism; Drug Delivery Systems/methods; Ileum/drug effects; Ileum/metabolism; Intestinal Mucosa/drug effects; Intestinal Mucosa/metabolism; Male; Potassium Channel Blockers/pharmacology; Potassium Channels/physiology; Propofol/pharmacology; Rats; Rats, Wistar; Drug Delivery Systems; Ileum; Intestinal Mucosa; Physiology; Endocrine and Autonomic Systems; Gastroenterology

Abstract :

[en] BACKGROUND: Propofol is a widely used intravenous general anesthetic. Acetylcholine (ACh) is critical in controlling epithelial ion transport. This study was to investigate the effects of propofol on ACh-evoked secretion in rat ileum epithelium. METHODS: The Ussing chamber technique was used to investigate the effects of propofol on carbachol (CCh)-evoked short-circuit currents (Isc). KEY RESULTS: Propofol (10-2 -10-6 mol/L) attenuated CCh-evoked Isc of rat ileum mucosa in a dose-dependent manner. The inhibitory effect of propofol was only evident after application to the serosal side. Pretreatment with tetrodotoxin (TTX, 0.3 μmol/L, n=5) had no effect on propofol-induced inhibitory effect, whereas serosal application of K+ channel inhibitor, glibenclamide, but not, an ATP-sensitive K+ channel inhibitor, largely reduced the inhibitory effect of propofol. In addition, pretreatment with either hexamethonium bromide (HB, nicotinic nACh receptor antagonist) or Cl- channel blockers niflumic acid and cystic fibrosis transmembrane conductance regulator (inh)-172 did not produce any effect on the propofol-induced inhibitory effect. CONCLUSIONS & INFERENCES: Propofol inhibits CCh-induced intestinal secretion by directly targeting basolateral K+ channels.

Disciplines :

Biochemistry, biophysics & molecular biology

Author, co-author :

Tang, S-H; Department of Anesthesiology, Qilu Hospital, Shandong University, Jinan, China

Wang, H-Y; Department of Physiology, School of Medicine, Shandong University, Jinan, China

Sun, H; Department of Thoracic Surgery, Shandong Tumor Hospital, Shandong University, Jinan, China

An, Ning ; Université de Liège - ULiège > GIGA > GIGA Stem Cells - Cancer Signaling ; Department of Physiology, School of Medicine, Shandong University, Jinan, China

Xiao, L; Department of Physiology, School of Medicine, Shandong University, Jinan, China

Sun, Q; Department of Physiology, School of Medicine, Shandong University, Jinan, China

Zhao, D-B; Department of Thoracic Surgery, Shandong Tumor Hospital, Shandong University, Jinan, China

Language :

English

Title :

Propofol inhibits carbachol-induced chloride secretion by directly targeting the basolateral K+ channel in rat ileum epithelium.

Publication date :

February 2017

Journal title :

Neurogastroenterology and Motility

ISSN :

1350-1925

eISSN :

1365-2982

Publisher :

Blackwell Publishing Ltd, England

Volume :

Issue :

Pages :

e12934

Peer reviewed :

Peer Reviewed verified by ORBi

Additional URL :

https://api.wiley.com/onlinelibrary/tdm/v1/articles/10.1111%2Fnmo.12934

Funders :

Shandong University

Funding text :

This study was granted by the Fundamental Research Funds of Shandong University (2014QLKY08). This work was supported by the Fundamental Research Funds of Shandong University (2014QLKY08).

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