Basic Science Research

Control of Microcirculatory Exchange Function
Walter N. Duran PhD

Inflammatory processes are characterized by an increase in microvascular permeability to macromolecules. Current information highlights controversial reports on the impact of nitric oxide (NO) in the control of microvascular permeability. Evidence in tissues and in isolated venules indicates that the activity of endothelial constitutive NO synthase (eNOS) increases microvascular permeability. To advance knowledge of the regulation of microvascular permeability, we are investigating three major hypotheses: 1) an eNOS-associated signaling cascade regulates microvascular transport; 2) molecular movement (translocation, trafficking) of eNOS from membrane to other cellular compartment(s) is a functionally and differentially important step in the endothelium-mediated regulatory mechanisms in vivo; and 3) eNOS signaling mechanisms regulate microvascular permeability. These studies are funded by the NIH.

Baseline distribution of eNOS (red) and caveolin (green) in human microvascular endothelial cells. Note preferential membrane-bound distribution of eNOS.