The ins and outs of endothelial dysfunction: much ado about NO-thing.

Overview

This article presents data linking eNOS function and nitric oxide (NO) generation or availability to vascular remodeling and signaling, hyperlipidemias, advanced glycated end products and hyperglycemia. These data should be viewed within the broader framework of endothelial cell dysfunction (ECD). It is possible that vascular dysfunctions are capable of triggering early preclinical forms of generalized ECD. Accordingly, it is important to learn more about simple noninvasive ways to assess the functional state of eNOS and the bioavailability of NO. Here we discuss the growing body of evidence--which suggests that disturbances of NO production or availability are major determinants of ECD--and the need for therapeutic efforts toward correction of eNOS activity and NO levels in blood vessels.