title: Small artery structure adapts to vasodilatation rather than to blood pressure during antihypertensive treatment.
abstract: OBJECTIVE
  Correction of the abnormal structure of resistance arteries in essential hypertension may be an important treatment goal in addition to blood pressure (BP) reduction. We investigated how this may be achieved in a prospective clinical study.
  
  
  METHODS
  Plethysmography was used to measure forearm resting vascular resistance (Rrest) and minimum vascular resistance (Rmin) as a measure of vascular structure. Two different groups of patients with essential hypertension were examined at baseline and after 6 months of antihypertensive treatment. In group A, 21 patients with never-treated essential hypertension were treated by their general practitioners using a variety of drugs to allow an assessment of the drug-independent effects. In group B, 28 beta-blocker-treated patients were shifted to angiotensin II receptor blocker treatment (eprosartan) to allow vasodilatation with no change in BP.
  
  
  RESULTS
  In group A, mean ambulatory blood pressure (ABP) fell from 119 +/- 2 (SE) to 103 +/- 2 mmHg (P < 0.01), whereas mean ABP was unchanged in group B (100 +/- 1 to 99 +/- 1 mmHg, P = NS). Both groups showed similar reductions in Rrest (-33.4 and -28.5%, respectively) and in Rmin (-15.4 and -15.6%, respectively). There was a strong correlation between changes in Rrest and Rmin within both groups (r = 0.57, P < 0.01 and r = 0.68, P < 0.0001, respectively), whereas the change in BP in group A was not correlated to the change in Rmin (r = -0.03).
  
  
  CONCLUSIONS
  The correction of forearm resistance artery structure during antihypertensive treatment depends on the vasodilatation achieved rather than BP reduction.
authors.affiliation: Department of Pharmacology, University of Aarhus, Denmark. onm@farm.au.dk
authors.forename: Ole N
authors.initials: ON
authors.lastname: Mathiassen
authors.forename: Niels H
authors.initials: NH
authors.lastname: Buus
authors.forename: Mogens L
authors.initials: ML
authors.lastname: Larsen
authors.forename: Michael J
authors.initials: MJ
authors.lastname: Mulvany
authors.forename: Kent L
authors.initials: KL
authors.lastname: Christensen
mesh_terms: D000179:Acrylates / Q000494:pharmacology; D000328:Adult; D000959:Antihypertensive Agents / Q000494:pharmacology*; D001158:Arteries / Q000187:drug effects*; D001794:Blood Pressure / Q000187:drug effects*; D016022:Case-Control Studies; D004452:Echocardiography; D005260:Female; D006801:Humans; D007093:Imidazoles / Q000494:pharmacology; D008297:Male; D008875:Middle Aged; D013876:Thiophenes / Q000494:pharmacology; D014655:Vascular Resistance / Q000187:drug effects*; D014664:Vasodilation / Q000187:drug effects*; D016277:Ventricular Function, Left / Q000187:drug effects
chemical_list: D000179:Acrylates; D000959:Antihypertensive Agents; D007093:Imidazoles; D013876:Thiophenes; C068373:eprosartan