Role of 20-HETE in the hypoxia-induced activation of Ca2+-activated K+ channel currents in rat cerebral arterial muscle cells

摘要

various physiological mechanisms protect the brain -from the deleterious effects of tissue hypoxia. One of these mechanisms is a reactive vasodilatory response of the cerebral vasculature that increases cerebral blood flow (CBF) to maintain O2 and energy supply to the brain under hypoxic conditions (4). This protective effect could be achieved through the action of hypoxia on vascular endothelial cells, on vascular smooth muscle cells, and on brain extravascular tissues such as neurons and astroglial cells (27). The roles of endothelial cells and neurons in elaborating the effects of hypoxia or reduced P02 have been well documented (27). Thus hypoxia has been reported to stimulate the release of various vasodilatory factors including nitric oxide, prostacyclin (PGI2), and endothelium-derived hyperpolarizing factor from endothelial cells, whereas in neuronal cells hypoxia induces release of hydrogen ion, K+ ion, adenosine, and the excitatory amino acids (27).