Nitric Oxide가 쥐 뇌에서 분리된 Ca2+-activated K+(Maxi-K) channel에 미치는 영향

초록

Nitric oxide(NO)has many roles in various tissues including cytotoxic effects of activated macrophages, decreases in cardiac contractility, and the regulation of the vascular tone. NO is also suggested as a neurotransmitter in brain. One of the mechanisms for NO action is through activating guanylate cyclase. Direct action of NO on many channel proteins have also been reported. The excised patches of vascular smooth muscle cells activated Maxi-K channels, and concluded that NO directly affects the channel activities. However, it is still arguable that the Maxi-K channel is activated indirectly since there could be some components in the patch membrane which might affect the channel activity through NO. We investigated the question whether NO directly affects the activities of the Maxi-K channels using the lipid bilayer reconstitution method. This method has advantages over the patch clamping. Firstly, it provides a relatively clean environment and can minimize the possibility of NO affecting the channel via other proteins in the bilayer. Secondly, the chances of obtaining single channel activity are far greater than the patch clamp method, which would give information regarding the molecular mechanism of NO action on channel protein.