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Role of Ca2+‐activated K+ channels in 11,12‐epoxyeicosatrienoic acid‐induced vasodilation of parenchymal arterioles: possible role of astrocytes

A current hypothesis suggests that glutamate‐induced Ca2+ changes in astrocytes leads to arachidonic acid mobilization and production and release of epoxyeicosatrienoic acids (EETs), which diffuse to smooth muscle cells and mediate vasodilation through their action on Ca2+‐activated K+ channels (BK channels). Here, we present an alternative hypothesis where EETs’ action in the neurovascular response is initiated at the level of the astrocytes, in particular the endfeet, resulting in BK channel activation contributing to K+‐induced vasodilation. Using confocal Ca2+ imaging techniques, electrophysiology and video microscopy from cortical brain slices, we observed a robust increase in astrocytic Ca2+in response to 11,12‐EET. Interestingly, while this response occurred rapidly (~2–15 sec), EET‐induced arteriolar dilation (~46% from baseline) was significantly delayed (~2 min), suggesting that the locus of EETs’ primary neurovascular action might be at the level of the astrocytes. In addition, we also observed a significant increase in whole‐cell outward currents from astrocytes in response to 11,12‐EET, and suppression of EET‐induced arteriolar dilation in the presence of the BK channel blocker TEA (1mM). Our data support the novel hypothesis that EETs, by increasing intracellular Ca2+ in astrocytes, may modulate BK channel activity and thus K+‐induced dilation of parenchymal arterioles.