title: Shear stress abnormalities contribute to endothelial dysfunction in hypertension but not in type II diabetes.
abstract: BACKGROUND
  The relative contribution of the various hemodynamic and metabolic mechanisms leading to endothelial dysfunction may be different in specific vascular diseases. Since shear stress is one of the main mechanical stimuli of endothelial cells, the aim of this study was to investigate its contribution to endothelial dysfunction in two distinct vascular diseases, hypertension and type II diabetes.
  
  
  METHODS
  We measured the radial artery diameter at baseline, after ischemic vasodilation and after nitroglycerin vasodilation in 16 untreated patients with high blood pressure, in 15 type II normotensive diabetic patients and in 17 healthy controls. Wall shear stress was evaluated by simultaneous measurements of whole blood viscosity and blood flow velocity.
  
  
  RESULTS
  In diabetic patients, whole blood viscosity was significantly higher whereas wall shear stress was similar compared to controls. In hypertensive patients, whole blood viscosity was higher and wall shear stress was lower than in controls. Endothelium-dependent vasodilation was impaired in both hypertensive and diabetic patients (P < 0.01) after adjustment for age, sex, body mass index and postnitroglycerin vasodilation. When adjustments were made for maximal systolic shear stress, endothelium-dependent vasodilation remained lower in the diabetic patients (P < 0.01), but not in those with high blood pressure compared to controls.
  
  
  CONCLUSIONS
  In hypertension, endothelium-dependent vasodilation is mainly due to a chronic decrease in shear stress (the most important physiological stimulus of the endothelial cells) with no major intrinsic endothelial cell dysfunction. In contrast, in diabetics, the lower endothelium-dependent vasodilation was not the result of an altered shear stress.
authors.affiliation: Centre d'Investigation Clinique INSERM-CHU, Nancy, France.
authors.forename: Y
authors.initials: Y
authors.lastname: Khder
authors.forename: S
authors.initials: S
authors.lastname: Briançon
authors.forename: R
authors.initials: R
authors.lastname: Petermann
authors.forename: D
authors.initials: D
authors.lastname: Quilliot
authors.forename: J F
authors.initials: JF
authors.lastname: Stoltz
authors.forename: P
authors.initials: P
authors.lastname: Drouin
authors.forename: F
authors.initials: F
authors.lastname: Zannad
mesh_terms: D000328:Adult; D001794:Blood Pressure; D001809:Blood Viscosity; D015992:Body Mass Index; D003627:Data Interpretation, Statistical; D003924:Diabetes Mellitus, Type 2 / Q000000981:diagnostic imaging / Q000503:physiopathology*; D004730:Endothelium, Vascular / Q000000981:diagnostic imaging / Q000503:physiopathology*; D005260:Female; D006442:Glycated Hemoglobin; D006439:Hemodynamics; D018056:Hemorheology; D006801:Humans; D006973:Hypertension / Q000000981:diagnostic imaging / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D013314:Stress, Mechanical; D014463:Ultrasonography
chemical_list: D006442:Glycated Hemoglobin