title: Vascular structural and functional changes in type 2 diabetes mellitus: evidence for the roles of abnormal myogenic responsiveness and dyslipidemia.
abstract: BACKGROUND
  To further investigate vascular morphology and function in type 2 (non-insulin-dependent) diabetes mellitus (type 2D), small arteries were examined in vitro from carefully defined cohorts of patients with or without concomitant hypertension and the results compared with those from selected normotensive nondiabetic control subjects and a group of untreated patients with essential hypertension (EH).
  
  
  RESULTS
  Blood vessels were studied through the use of pressure myography to determine vascular morphology, mechanics, and myogenic responsiveness, together with testing of constrictor and dilator function. Small arteries from patients with EH demonstrated eutrophic inward remodeling and an increased distensibility. Vessels from type 2D patients demonstrated hypertrophy, a further increase in distensibility, and a highly significant loss of myogenic responsiveness compared with patients with EH and control patients. Vasoconstrictor function to norepinephrine was normal in patients with type 2D and type 2D+H and EH. Endothelium-dependent dilation was normal in patients with EH but abnormal in patients with type 2D and type 2D+H. There was a significant correlation between dilator impairment and the degree of dyslipidemia recorded in all groups.
  
  
  CONCLUSIONS
  These results demonstrate vascular hypertrophy in small arteries from patients with type 2D. This could be a consequence of impaired myogenic responsiveness, which will increase wall stress for a given intraluminal pressure, which may be a stimulus for vascular hypertrophy. A substantial proportion of endothelial dysfunction can be attributed to an effect of the abnormal lipid profile seen in such patients.
authors.affiliation: Cardiovascular Research Group, Department of Medicine, Manchester Royal Infirmary, Manchester, UK.
authors.forename: Ian
authors.initials: I
authors.lastname: Schofield
authors.forename: Rayaz
authors.initials: R
authors.lastname: Malik
authors.forename: Ashley
authors.initials: A
authors.lastname: Izzard
authors.forename: Clare
authors.initials: C
authors.lastname: Austin
authors.forename: Anthony
authors.initials: A
authors.lastname: Heagerty
mesh_terms: D000273:Adipose Tissue / Q000098:blood supply; D001158:Arteries / Q000187:drug effects / Q000473:pathology / Q000503:physiopathology*; D001794:Blood Pressure; D002784:Cholesterol / Q000097:blood; D015331:Cohort Studies; D003924:Diabetes Mellitus, Type 2 / Q000150:complications / Q000503:physiopathology*; D004305:Dose-Response Relationship, Drug; D004837:Epinephrine / Q000494:pharmacology; D005260:Female; D006801:Humans; D006949:Hyperlipidemias / Q000097:blood* / Q000150:complications; D006973:Hypertension / Q000150:complications / Q000503:physiopathology*; D066298:In Vitro Techniques; D008297:Male; D008875:Middle Aged; D009129:Muscle Tonus / Q000187:drug effects; D009599:Nitroprusside / Q000494:pharmacology; D013314:Stress, Mechanical; D014661:Vasoconstriction / Q000187:drug effects; D014662:Vasoconstrictor Agents / Q000494:pharmacology; D014664:Vasodilation / Q000187:drug effects; D014665:Vasodilator Agents / Q000494:pharmacology
chemical_list: D014662:Vasoconstrictor Agents; D014665:Vasodilator Agents; D009599:Nitroprusside; D002784:Cholesterol; D004837:Epinephrine