tion of external potassium, the activity of these channels increases, causing smooth muscle cells to become less excitable, resulting in relaxation of the cells, dilation of vessels, and hence an increase in local blood flow. Similar to the BK channel, it was found that a reduction of inward rectifier channels prevented dilation of vessels in response to neuronal activity.
These findings support the novel concept that precise and spatially localized release of potassium ions from astrocytes onto blood vessels mediates the rapid transmission of neuronal activity into regional increases in blood flow.
In addition, this mechanism places into a physiological context the well characterized responsiveness of the cerebral circulation to changes in extracellular potassium, and suggests that alterations in astrocytic BK channel or smooth muscle cell inward rectifier potassium channel function could contribute to cerebrovascular disorders including local cerebral ischemia, dementia and Alzheimer’s disease.
This study suggests that these proteins may be novel targets to protect the brain from cerebrovascular disorders. In addition to Nelson, the research team included Jessica Filosa, Ph.D., postdoctoral fellow in pharmacology; Adrian Bonev, Ph.D., research assistant professor of pharmacology; Stephen Straub, Ph.D., postdoctoral fellow in pharmacology; Keith Wilkerson, Ph.D., postdoctoral fellow in pharmacology; and collaborators at Stanford University.
As a follow up to this work, Nelson and Straub published a study in the December 2006 issue of the Journal of General Physiology that investigated the spatial and temporal characteristics of the calcium signals within astrocytic endfeet, and defined the spatial context of vasoactive signals generated by endfeet. This vasodilation was restricted to a short stretch of the vessel centered on the endfoot, suggesting that endfeet function as individual “vasoregulatory units” in the brPage: 1 2 3 4 Related medicine news :1
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