Nitric oxide affects microvascular permeability in the intact and inflamed vasculature.
There is a growing body of evidence that nitric oxide modulates the movement of fluid and protein out of the vasculature. However, the results obtained from whole organ, single vessel, and endothelial monolayer studies are often not consistent. In fact, there is much evidence that endogenous nitric oxide increases microvascular permeability and equally compelling evidence to suggest that endogenous nitric oxide decreases microvascular permeability. In this review we summarize and critically evaluate the data published to date regarding the role of nitric oxide as a modulator of microvascular permeability under both normal conditions and following exposure to various stimuli. The last section of the chapter discusses the importance of nitric oxide as a modulator of microvascular permeability in inflammatory conditions. Particular emphasis is placed on the stimuli used, the organ systems studied, and the measurements performed to investigate the effects of nitric oxide on microvascular permeability alterations.
Kubes
P
P
Department of Physiology, University of Calgary Medical Center, Alberta, Canada.
D000818:Animals; D002199:Capillary Permeability; D006801:Humans; D007249:Inflammation / Q000503:physiopathology; D008833:Microcirculation / Q000502:physiology*; D009569:Nitric Oxide / Q000096:biosynthesis / Q000502:physiology*
D009569:Nitric Oxide