title: Endothelial dysfunction in resistance arteries is related to high blood pressure and circulating low density lipoproteins in previously treated hypertension.
abstract: BACKGROUND
  Peripheral endothelial dysfunction has been demonstrated in hypertension. However, its relationship to blood pressure (BP) load, vascular structure, and metabolic disturbances in patients with long-standing, previously treated hypertension is unclear.
  
  
  METHODS
  A total of 41 patients with stage I to III essential hypertension and electrocardiographic left ventricular hypertrophy were studied. After 2 to 3 weeks of placebo treatment we measured nitroprusside-induced relaxation (NIR), acetylcholine-induced relaxation (AIR), and media:lumen ratio in isolated, subcutaneous resistance arteries by myography, as well as 24-h ambulatory BP, and serum lipids.
  
  
  RESULTS
  Maximal AIR correlated negatively with median 24-h diastolic BP (r=-0.42, P=.01), and sensitivity to AIR correlated negatively with serum low density lipoprotein (LDL) (r =-0.36, P < .05). In multiple regression analyses, sensitivity to AIR correlated negatively with serum LDL (beta=-0.33) independently of maximal NIR (beta=0.41) (adjusted R2 =0.26, P < .01). Maximal acetylcholine-induced relaxation correlated negatively with median 24-h diastolic BP (beta=-0.38) independently of maximal NIR (beta=0.45) (adjusted R2= 0.32, P < .001). Acetylcholine-induced relaxation was not significantly related to diabetes or to media:lumen ratio (r = -0.26, NS).
  
  
  CONCLUSIONS
  High diastolic BP and high serum LDL were associated with impaired maximal AIR and reduced sensitivity to AIR, respectively, independently of smooth muscle cell responsiveness to nitroprusside. This indicated decreasing endothelial function in small resistance arteries with increasing BP and increasing LDL in hypertension. Endothelial function was not significantly related to vascular structure of the resistance arteries or to diabetes in these patients with long-standing hypertension.
authors.affiliation: Department of Clinical Physiology and Nuclear Medicine, Glostrup Hospital, University of Copenhagen,  Denmark. mho@dadlnet.dk
authors.forename: M H
authors.initials: MH
authors.lastname: Olsen
authors.forename: K
authors.initials: K
authors.lastname: Wachtell
authors.forename: C
authors.initials: C
authors.lastname: Aalkjaer
authors.forename: R B
authors.initials: RB
authors.lastname: Devereux
authors.forename: H
authors.initials: H
authors.lastname: Dige-Petersen
authors.forename: H
authors.initials: H
authors.lastname: Ibsen
mesh_terms: D000109:Acetylcholine / Q000494:pharmacology; D000368:Aged; D001158:Arteries / Q000187:drug effects / Q000503:physiopathology*; D001775:Blood Circulation / Q000502:physiology*; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D002940:Circadian Rhythm / Q000502:physiology; D004730:Endothelium, Vascular / Q000503:physiopathology*; D005260:Female; D006801:Humans; D006973:Hypertension / Q000097:blood* / Q000150:complications*; D017379:Hypertrophy, Left Ventricular / Q000097:blood / Q000150:complications; D008077:Lipoproteins, LDL / Q000097:blood*; D008297:Male; D008875:Middle Aged; D009126:Muscle Relaxation / Q000187:drug effects / Q000502:physiology; D009599:Nitroprusside / Q000494:pharmacology; D012044:Regression Analysis; D012680:Sensitivity and Specificity; D012907:Smoking / Q000009:adverse effects; D014655:Vascular Resistance / Q000187:drug effects / Q000502:physiology*
chemical_list: D008077:Lipoproteins, LDL; D009599:Nitroprusside; D000109:Acetylcholine