This review has summarized experiments which show that the connective tissue cells can actively modulate the physical properties of the interstitial matrix so that it becomes an "active" participant in transcapillary fluid exchange and thereby interstitial fluid homeostasis. The beta1-integrin system seems to provide a common pathway by which the cells can both raise and lower the interstitial fluid pressure. The experiments with alpha-trinositol and platelet-derived growth factor-BB suggest that the connective tissue can serve as a novel target for pharmacologic intervention in inflammation.
Copyright 2001 by W.B. Saunders Company