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B inhibitors in colonic smooth muscle isolated from a TNBS-induced colitis model rat
1 Department of Vetterinary Pharmacology, The University of Tokyo, Tokyo, Japan, Japan
* To whom correspondence should be addressed. E-mail: aozaki{at}mail.ecc.u-tokyo.ac.jp.
We investigated the mechanisms of dysmotility of the colonic circular muscle of the Crohn's disease model rat. Contractions induced by KCl, carbachol, and Bay K 8644 were decreased in circular smooth muscles isolated from TNBS-induced colitis rat colon. However, the absolute force and Ca2+ sensitivity of contractile proteins were not affected as assessed in alpha-toxin permeabilized smooth muscle. The current density of the L-type Ca2+-channel in circular smooth muscle cells was significantly decreased in the TNBS-treated colonic cells. However, expressions of the L-type Ca2+-channel mRNA and protein did not differ between control and TNBS-treated preparations. Pretreatment with NF-
B inhibitors, pyrroplidine dithocarbamate (PDTC) and sulfasalazine, partially recovered the decreased contractility and current density of the L-type Ca2+-channel by TNBS treatment. These results suggest that the decrease in the contraction of circular smooth muscle isolated from TNBS-induced colitis rat colon, which may be related to gut dysmotility in Crohn's disease, is attributable to the decreased activity of the L-type Ca2+-channel. The dysfunction of the L-type Ca2+-channel may be mediated by NF-B-dependent pathways.
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