title: Control of interstitial fluid pressure: role of beta1-integrins.
abstract: 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.
authors.affiliation: Department of Physiology, University of Bergen, Norway.
authors.forename: R K
authors.initials: RK
authors.lastname: Reed
authors.forename: A
authors.initials: A
authors.lastname: Berg
authors.forename: E A
authors.initials: EA
authors.lastname: Gjerde
authors.forename: K
authors.initials: K
authors.lastname: Rubin
mesh_terms: D000818:Animals; D003239:Connective Tissue Cells / Q000502:physiology; D005110:Extracellular Space / Q000502:physiology*; D006168:Guinea Pigs; D006874:Hydrostatic Pressure; D007249:Inflammation / Q000503:physiopathology*; D019012:Integrin beta1 / Q000502:physiology*; D009997:Osmotic Pressure; D051381:Rats; D015398:Signal Transduction / Q000502:physiology; D014882:Water-Electrolyte Balance / Q000502:physiology
chemical_list: D019012:Integrin beta1