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CO stimulates the Ca2+ –activated big conductance K (BK) channels in human endothelial cells
Author(s) -
Dong Deli,
Chen Jun,
Patschan Susann,
Goligorsky Michael,
Nasjletti Alberto,
Yang Baofeng,
Wang Wenhui
Publication year - 2007
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.21.5.a522-c
Subject(s) - bk channel , iberiotoxin , chemistry , umbilical vein , sodium nitroprusside , calcium activated potassium channel , stimulation , biophysics , patch clamp , microbiology and biotechnology , endocrinology , nitric oxide , membrane potential , biochemistry , receptor , calcium , biology , in vitro , organic chemistry
We used the patch‐clamp technique to study the effect of CO on K channels in the human umbilical vein endothelial cell (HUVEC). Application of CO or CORM3 (CO donor) stimulates a 200 pS K channels which are activated by raising cell Ca2+ and blocked by TEA and iberiotoxin. This suggests that BK channels are present in HUVEC and activated by CO. Also, BK channel activity is stimulated by application of sodium nitroprusside (SNP), a NO donor. To determine whether the stimulatory effect of CO on BK channels was the result of increasing NO release, we examined the effect of CO on BK channels in the cells treated with L‐NAME to block endogenous NOS. In the presence of L‐NAME, application of either CO or CORM3 still increased the BK channel activity. However, inhibition of NOS has significantly prolonged the onset time of CO‐induced stimulation of BK channels. This suggests that the early effect of CO may be due to increasing NO release. We next investigated the effect of CO on BK channels in the endothelial cells treated with ODQ. Inhibition of soluable guanylate cyclase did not abolish the stimulatory effect of CO on BK channels. We conclude that BK channels are expressed in human endothelial cells and activated by CO and NO. Also, CO activates BK channels by a NO and cGMP‐independent pathway.