title: Excessive microvascular adaptation to changes in blood flow in mice lacking gene encoding for desmin.
abstract: OBJECTIVE
  Desmin, an intermediate filament, has a key role in the integrity of myocytes, and its absence induces cardiomyopathies. Mice lacking desmin (Des-/- group) exhibit microvascular dysfunction leading to smooth muscle hyporeactivity. We investigated the effect of the absence of desmin in mice (Des-/- mice versus Des+/+ mice) on the adaptation of mesenteric arteries to changes in blood flow.
  
  
  RESULTS
  With the use of selective ligations of second-order mesenteric arteries, blood flow was either diminished (low flow [LF]) or elevated (high flow [HF]); respective LF to HF values were 136+/-18 to 206+/-29 microL/min for Des+/+ mice and 119+/-14 to 189+/-24 microL/min for Des-/-mice in daughter arteries. Two weeks after ligation, arteries were mounted in an arteriograph, allowing the measurement of diameter under controlled conditions of pressure and flow. In HF arteries, diameter changes in response to increases in pressure were higher in Des-/- mice than in Des+/+ mice. Conversely, in LF arteries, diameter was lower in Des-/- mice. Flow-dependent dilation was higher in HF arteries and lower in LF arteries than in control arteries. This adaptation was lower in Des-/- mice than in Des+/+ mice (11.6+/-3.1% versus 25.5+/-4.8% dilation, respectively). Endothelial NO synthase expression increased in HF arteries in both strains.
  
  
  CONCLUSIONS
  These findings provide a demonstration of the role of the intermediate filament desmin in microvascular remodeling. This dysfunction might take place in desmin-related myopathies.
authors.affiliation: Institut National de la Santé et de la Recherche Médicale U 541, IFR Circulation-Paris-Nord, Paris, France.
authors.forename: Laurent
authors.initials: L
authors.lastname: Loufrani
authors.forename: Zhenlin
authors.initials: Z
authors.lastname: Li
authors.forename: Bernard I
authors.initials: BI
authors.lastname: Lévy
authors.forename: Denise
authors.initials: D
authors.lastname: Paulin
authors.forename: Daniel
authors.initials: D
authors.lastname: Henrion
mesh_terms: D000222:Adaptation, Physiological / Q000235:genetics* / Q000502:physiology; D000818:Animals; D003893:Desmin / Q000172:deficiency* / Q000235:genetics* / Q000502:physiology; D004730:Endothelium, Vascular / Q000378:metabolism / Q000502:physiology / Q000601:surgery; D008026:Ligation / Q000379:methods; D008297:Male; D008638:Mesenteric Arteries / Q000378:metabolism / Q000601:surgery; D051379:Mice; D008817:Mice, Mutant Strains; D008833:Microcirculation / Q000378:metabolism / Q000503:physiopathology; D009131:Muscle, Smooth, Vascular / Q000098:blood supply / Q000502:physiology / Q000601:surgery; D009135:Muscular Diseases / Q000235:genetics / Q000503:physiopathology; D012039:Regional Blood Flow / Q000235:genetics* / Q000502:physiology
chemical_list: D003893:Desmin