title: The protective effects of angiotensin II blockade with olmesartan medoxomil on resistance vessel remodeling (The VIOS study): rationale and baseline characteristics.
abstract: BACKGROUND
  The VIOS (Vascular Improvement with Olmesartan medoxomil Study) study is a randomized, parallel study to determine the relative effects of suppressing the renin-angiotensin system (RAS) with the angiotensin receptor antagonist olmesartan medoxomil versus suppressing sympathetic drive with the beta-adrenoceptor antagonist atenolol on remodeling of the subcutaneous small resistance vessel. Remodeling of small resistance vessels may be the earliest pathologic finding associated with hypertension. It may predate the onset of clinically apparent hypertension.
  
  
  METHODS
  In this study, 100 patients with stage I hypertension are characterized at baseline before being treated for 1 year to obtain a goal BP of less than 140/90 mm Hg as defined by Joint National Committee (JNC)-7. Resistance vessel remodeling is determined using the gluteal fat biopsy technique in the hypertensive patients and a group of normotensive healthy volunteers. Additionally, efforts will be made to define whether noninvasive hemodynamic parameters, retinal vessel measurement changes, or biologic markers may predict and track the underlying vascular morphologic and physiologic changes induced by either regimen during the 12-month treatment period.
  
  
  RESULTS
  The primary endpoint will be the degree of vascular remodeling as obtained from percutaneous biopsy of gluteal subcutaneous resistance vessels in each of two treatment arms compared with the normal volunteers. The design of the study and the pertinent baseline characteristics of these patients with uncomplicated essential hypertension are presented.
  
  
  CONCLUSIONS
  The suppression of the RAS by the blockade of angiotensin II type 1 (AT(1)) receptors may demonstrate remodeling effects on the ubiquitous small resistance vessels similar to that seen in the myocardium and renal glomeruli, thus affording more complete end-organ protection.
authors.affiliation: Hypertension and Vascular Disease Center, Wake Forest University School of Medicine, Winston Salem, North Carolina, USA. rosmith@wfubmc.edu
authors.forename: Ronald D
authors.initials: RD
authors.lastname: Smith
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Yokoyama
authors.forename: David B
authors.initials: DB
authors.lastname: Averill
authors.forename: Lori
authors.initials: L
authors.lastname: Cooke
authors.forename: K Bridget
authors.initials: KB
authors.lastname: Brosnihan
authors.forename: Ernesto L
authors.initials: EL
authors.lastname: Schiffrin
authors.forename: Carlos M
authors.initials: CM
authors.lastname: Ferrario
mesh_terms: D000328:Adult; D047228:Angiotensin II Type 1 Receptor Blockers / Q000008:administration & dosage / Q000627:therapeutic use*; D000959:Antihypertensive Agents / Q000008:administration & dosage / Q000627:therapeutic use; D001160:Arterioles / Q000187:drug effects* / Q000503:physiopathology; D015415:Biomarkers / Q000097:blood / Q000652:urine; D001794:Blood Pressure / Q000187:drug effects; D004359:Drug Therapy, Combination; D005260:Female; D006801:Humans; D006973:Hypertension / Q000175:diagnosis / Q000188:drug therapy* / Q000503:physiopathology; D007093:Imidazoles / Q000008:administration & dosage / Q000627:therapeutic use*; D008297:Male; D008875:Middle Aged; D000068557:Olmesartan Medoxomil; D012084:Renin-Angiotensin System / Q000187:drug effects / Q000502:physiology; D013777:Tetrazoles / Q000008:administration & dosage / Q000627:therapeutic use*; D016896:Treatment Outcome; D014655:Vascular Resistance / Q000187:drug effects
chemical_list: D047228:Angiotensin II Type 1 Receptor Blockers; D000959:Antihypertensive Agents; D015415:Biomarkers; D007093:Imidazoles; D013777:Tetrazoles; D000068557:Olmesartan Medoxomil