Heme is a carbon monoxide receptor for large-conductance Ca2+-activated K+ channels.

ABSTRACT: Carbon monoxide (CO) is an endogenous paracrine and autocrine gaseous messenger that regulates physiological functions in a wide variety of tissues. CO induces vasodilation by activating arterial smooth muscle large-conductance Ca2+-activated potassium (BK(Ca)) channels. However, the mechanism by which CO activates BK(Ca) channels remains unclear. Here, we tested the hypothesis that CO activates BK(Ca) channels by binding to channel-bound heme, a BK(Ca) channel inhibitor, and altering the interaction between heme and the conserved heme-binding domain (HBD) of the channel alpha subunit C terminus. Data obtained using thin-layer chromatography, spectrophotometry, mass spectrometry (MS), and MS-MS indicate that CO modifies the binding of reduced heme to the alpha subunit HBD. In contrast, CO

SUBMITTER: Jaggar JH 

PROVIDER: S-EPMC1415201 | biostudies-literature | 2005 Oct

REPOSITORIES: biostudies-literature