NO stimulation of ATP-sensitive potassium channels: Involvement of Ras/mitogen-activated protein kinase pathway and contribution to neuroprotection.

ABSTRACT: ATP-sensitive potassium (K(ATP)) channels regulate insulin release, vascular tone, and neuronal excitability. Whether these channels are modulated by NO, a membrane-permeant messenger in various physiological and pathological processes, is not known. The possibility of NO signaling via K(ATP) channel modulation is of interest because both NO and K(ATP) have been implicated in physiological functions such as vasodilation and neuroprotection. In this report, we demonstrate a mechanism that leads to K(ATP) activation via NO/Ras/mitogen-activated protein kinase pathway. By monitoring K(ATP) single-channel activities from human embryonic kidney 293 cell-attached patches expressing sulfonylurea receptor 2B and Kir6.2, we found K(ATP) stimulation by NO donor Noc-18, a specific NO effect abolished

SUBMITTER: Lin YF 

PROVIDER: S-EPMC419686 | biostudies-literature | 2004 May

REPOSITORIES: biostudies-literature