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ANTECEDENT HYDROGEN SULFIDE ELICITS AN ANTI‐INFLAMMATORY PHENOTYPE IN POSTISCHEMIC MURINE SMALL INTESTINE: ROLE OF BK Ca CHANNEL
Author(s) -
Yusof Mozow,
Yang Yan,
Davis Michael J.,
Korthuis Ronald J.
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.730.37
Subject(s) - bk channel , chemistry , inflammation , ischemia , biophysics , pharmacology , microbiology and biotechnology , immunology , medicine , biochemistry , biology , membrane potential
We recently demonstrated that preconditioning with an exogenous hydrogen sulfide (H 2 S) donor (NaHS‐PC) 24 h prior to ischemia and reperfusion (I/R) causes postcapillary venules to shift to an anti‐inflammatory phenotype in C57Bl/6 wild‐type mice such that these vessels fail to support leukocyte rolling (LR) and leukocyte adhesion (LA) during reperfusion. The objective of the present study was to determine whether the calcium‐sensitive large conductance K channel (BK Ca channel) is also involved as an initiator of the anti‐inflammatory phenotype elicited by H 2 S. The postischemic anti‐inflammatory effects of NaHS‐PC were abolished by BK Ca channel inhibitor treatment (paxilline) when administered coincident with NaHS, 24 hrs prior to I/R. Moreover, preconditioning with the BK Ca channel activator, NS‐1619, was as effective as NaHS‐PC in preventing I/R‐induced leukocyte rolling and adhesion. Our data is consistent with the concept that H 2 S induces the development of an anti‐adhesive state in I/R by a BK Ca channel‐dependent mechanism. (Patch‐clamp studies are presented separately). Supported by AA14945, DK43785 and HL71796