Mathias Oelze

TL;DR: In vivo and in vitro studies have indicated a crucial role of the diacylglycerol-protein kinase C (PKC) pathway in mediatingHyperglycemia is the major causal factor in the development of endothelial dysfunction in patients with diabetes mellitus.

TL;DR: It is concluded that angiotensin II-induced increases in the activity and the expression of NAD(P)H oxidase are at least in part PKC-dependent and may trigger NOS III uncoupling, leading to impaired NO/cGMP signaling and to endothelial dysfunction in this animal model.

TL;DR: NTG treatment increases the expression of a dysfunctional NOS III gene, leading to increased formation of O(2)(.-) and decreased vascular NO bioavailability, and an important role for PKC isoforms in mediating vascular dysfunction caused by long-term NTG treatment is suggested.

TL;DR: It is concluded that long-term NTG treatment induces endothelial dysfunction and impaired vascular NO/cGMP signaling in humans, which can be monitored by measuring P-VASP levels.

TL;DR: Pharmacologic interventions that combine eNOS up-regulation and reversal of eN OS uncoupling can markedly increase bioactive NO in the vasculature and produce beneficial hemodynamic effects such as a reduction of blood pressure.