Review
Contractile elements in endothelial cells as potential targets for drug action

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Abstract

It is now evident that vascular permeability to macromolecules is subject to a direct pressure-independent physiological and pharmacological regulation. Mediator-stimulated increases in vascular permeability and edema formation may be prevented by treatment with endothelial cell stabilizers which function as physiological mediator antagonists. These unique anti-permeability agents inhibit increases in vascular permeability produced by various inflammatory mediators. Since large junctional gap formation in venules is a characteristic feature of inflammation and so many chemically diverse inflammatory mediators participate in inflammatory responses, the development of a novel class of anti-inflammatory agents which act directly on the venular endothelial cell to inhibit mediator-stimulated increases in vascular permeability may well be warranted. George Grega reviews the evidence for supporting this proposal.

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