Impaired cross-talk between NO and hyperpolarization in myoendothelial feedback: a novel therapeutic target in early endothelial dysfunction of metabolic disease.

摘要: Over the past three decades, our view of endothelium rapidly evolved from a static lining blood vessels to dynamic determinant and regulator vascular tone homeostasis. It is now widely accepted that endothelial dysfunction hallmark almost every pathology, either as cause or consequence. The tight association between metabolic disease spectrum, ranging mild alterations lipids profile all way diabetes morbid obesity; complications argues for deleterious remodeling in these conditions. Extensive research demonstrated changes conditions including reduced nitric oxide activity, altered response endothelium-dependent hyperpolarization, increased production contractile agents. For most part, studies investigated different aspects function isolation each other. In this review, we propose model an integrated offer alternative potential early course continuum. such framework, only slight expression/function molecular players one pathway would be sufficient trigger cascade events compromising function. We will also consider available data describing possible effects intervention with therapeutic agents on disease.