Channelpedia

PubMed 22884438


Referenced in Channelpedia wiki pages of: none

Automatically associated channels: Kv10.1 , TRP , TRPV , TRPV1



Title: Role of KATP channels and TRPV1 receptors in hydrogen sulfide-enhanced gastric emptying of liquid in awake mice.

Authors: Jand Venes R Medeiros, Víctor H Bezerra, Larisse T Lucetti, Roberto César P Lima-Júnior, André Luiz R Barbosa, Bruno M Tavares, Pedro Jorge C Magalhães, Armênio A Santos, Fernando Q Cunha, Pedro Marcos G Soares, Marcellus H L P Souza

Journal, date & volume: Eur. J. Pharmacol., 2012 Oct 15 , 693, 57-63

PubMed link: http://www.ncbi.nlm.nih.gov/pubmed/22884438


Abstract
Hydrogen sulphide (H(2)S) has shown to relax gastrointestinal muscle. Here in, we evaluated the effects of H(2)S donors on gastric emptying and in pyloric sphincter muscle relaxation, and whether these effects involved K(ATP) channels or TRPV1 receptors. Mice were treated with l-cysteine (alone or with propargylglycine-an inhibitor of H(2)S synthesis), NaHS, Lawesson's reagent (H(2)S donors) or saline. After 30 min, mice were gavaged with a liquid meal containing a nonabsorbable marker and then killed at 10, 20 or 30 min intervals to assess marker recovery from the stomach and intestine. This experiment was repeated in mice pre-treated with K(ATP) channel (glibenclamide) or TRPV1 receptor (capsazepine) antagonists. In addition, pyloric sphincter muscles were mounted in an organ bath, incubated with saline, glibenclamide or capsazepine, and NaHS dose-responses were determined. H(2)S donors and l-cysteine enhanced gastric emptying in a dose-dependent manner; propargylglycine reversed the effect of l-cysteine. Both glibenclamide and capsazepine abolished l-cysteine and H(2)S donors' augmentation of gastric emptying. Dose-dependent inductions of pyloric sphincter relaxation by NaHS were abolished by glibenclamide or capsazepine. These data suggest that H(2)S donors-induced acceleration of gastric emptying and relaxation of pyloric sphincter muscle by K(ATP) channel and TRPV1 receptor activations.