The Resveratrol-induced Relaxation of Cholecystokinin Octapeptide- or KCl-induced XXXX in Male @entity840 Gallbladder Strips Is Mediated Through L-type Ca(2+) Channels.

@entity2701 @entity840 @entity1129
Background/Aims: Resveratrol (3,5,4'-trihydroxystilbene) is a polyphenolic compound (stilbene) and a phytoalexin. The purpose of this study was to determine the mechanism which mediated the resveratrol-induced relaxation of cholecystokinin octapeptide- or KCl-induced @entity2701 in male @entity840 gallbladder strips. Methods: Gallbladder strips were prepared and suspended in in vitro chambers filled with Krebs-Henseleit solution. The strips were attached to force displacement transducers, and the changes in @entity2701 were recorded on a polygraph. All reagents were added directly into the chambers. Results: To determine if intracellular Ca(2+) release mediated the resveratrol-induced relaxation of cholecystokinin octapeptide-induced @entity2701 , 2-aminoethoxydiphenylborane (2-APB) was used. 2-APB significantly (P < 0.01) decreased the amount of RSVL-induced relaxation. To determine if @entity1129 ( @entity1129 ) mediated the resveratrol-induced relaxation, @entity1129 inhibitor 14-22 amide myristolated ( @entity1129 -IM) was used. @entity1129 -IM had no effect on resveratrol-induced relaxation. Neither KT5823, N(G)-methyl-L-arginine acetate salt, a nitric oxide synthase inhibitor, nor fulvestrant had a significant effect on the amount of resveratrol-induced relaxation. Genistein, a protein tyrosine kinase inhibitor, significantly (P < 0.01) increased the RSVL-induced relaxation. To determine if protein kinase C mediated the RSVL-induced relaxation, the protein kinase C inhibitors bisindolymaleimide IV and chelerythrine Cl- were used together, and a significant (P < 0.05) increase in resveratrol-induced relaxation was observed. The pretreatment of the strips with resveratrol significantly (P < 0.001) decreased the amount of KCl- and cholecystokinin octapeptide- induced @entity2701 . Conclusions: Resveratrol-induced relaxation is mediated by its effects on L-type Ca(2+) channels and intracellular Ca(2+) release.
