Axel Gödecke

TL;DR: HDL is identified as a carrier of bioactive lysophospholipids that regulate vascular tone via S1P3-mediated NO release and induces vasodilation in isolated aortae via intracellular Ca2+ mobilization and Akt-mediated eNOS phosphorylation.

TL;DR: Evidence is provided for a uniform constitutive vascular NOS-activity across mammalian species by determining plasma nitrite concentration to be in a nanomolar range in a variety of species.

TL;DR: Evidence is provided that RBCs from humans express an active and functional endothelial-type NOS (eNOS), which is localized in the plasma membrane and the cytoplasm of R BCs, which is regulated by its substrate L-arginine, by calcium, and by phosphorylation via PI3 kinase.

TL;DR: The data indicate that this cycle is crucial in the breakdown of NO and substantially determines the dose-response curve of the NO effects on coronary blood flow and cardiac contractility.

TL;DR: Results demonstrate that in murine resistance vessels the predominant agonist-induced endothelium-dependent vasodilation in vivo and in vitro is not mediated by NO, PGI(2), or a cytochrome P450 metabolite, but by an EDHF-like principle that requires functional gap junctions.