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AM-induced endothelium-dependent vasodilation is mediated by PI3K/Art/NO/cGMP pathway, the activation of cGMP-stimulated protein kinase G and/or the production of a vasodilator prostanoid (likely prostacyclin)[42,45,46], whereas AM-induced endothelium-independent vasodilation involves the opening of K + channels (calcium-activated K + channels or ATP sensitive K + channels, probably depending upon vascular beds) and the activation of cAMP-dependent protein kinase A[42,47]

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However, the remaining sodium-dependent uptake that was not DHK sensitive can be attributed to the glutamate transporter, EAAT3

[DOI] [PMC free article] [PubMed] 33.Krause MS, Oliveira LP, Silveira EMS, Vianna DR, Rossato JS, Almeida BS, et al

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