eNOS

eNOS (NOS3) generates endothelial nitric oxide (NO), a vasoprotective signal that regulates vascular tone, blood pressure, platelet aggregation, leukocyte adhesion, and vascular homeostasis[1][2]. Mechanistically, Akt/PKB activates eNOS through Ser1177 phosphorylation, while agonist-stimulated endothelial cells integrate Ser1177 activation with Thr495 regulation to control NO output[3]. In disease models, eNOS loss or inhibition reduces endothelial NO signaling and increases blood pressure, as shown in eNOS-deficient mice and L-arginine/NOS inhibitor studies[4][5][6]. Compared with related isoforms, eNOS is mostly expressed in endothelial cells, nNOS mediates neuronal signaling, and iNOS produces high-output NO during inflammatory activation[1]. For experimental applications, L-NMMA, L-NIO, and L-NAME inhibit NOS activity and provide pharmacological tools to test endothelial NO-dependent vascular responses[6].
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