Nevertheless, the interactions between cAMP and EFAs are multifaceted. The functional effects of EETs acting through a cAMP pathway are extensively studied in the vasculature [40]. EETs are endothelium-derived hyperpolarizing factors (EDHF) in smooth muscle cells where the activity is mediated via Gαs stimulation, adenylyl cyclase (AC) activation, and subsequent increased cAMP [63]. The elevated cAMP results in activated BKCA channels which induce relaxation of coronary arteries. Similarly, in renal vasculature an EET mediated Gαs ADP ribosylation leads to AC activation, cAMP increases and by activating PKA prompts the dilation of microvessels [64]. Furthermore, EETs also mediate TRP channel translocation to plasma membranes [49]. It is unclear if these findings in the vasculature directly apply to neurons.
