title: Endothelial-dependent flow-mediated dilation in African Americans with masked-hypertension.
abstract: BACKGROUND
  Office-blood pressure (BP) measurements alone overlook a significant number of individuals with masked-hypertension (office-BP: 120/80-139/89 mm Hg and 24-h ambulatory BP monitoring (ABPM) daytime ≥135/85 mm Hg or night-time ≥120/70 mm Hg). Diminished endothelial function contributes to the pathogenesis of hypertension. To better understand the pathophysiology involved in the increased cardiovascular (CV) disease risk associated with masked-hypertension, we estimated the occurrence, assessed the endothelial function, compared plasma levels of inflammatory markers, white blood cell count (WBC count), tumor necrosis factor-α (TNF-α), and high sensitivity C-reactive protein (hsCRP) and examined the possible relationship between endothelial function and inflammatory markers in apparently healthy prehypertensive (office-BP: 120/80-139/89 mm Hg) African Americans.
  
  
  METHODS
  Fifty African Americans who were sedentary, nondiabetic, nonsmoking, devoid of CV disease were recruited. Office-BP was measured according to JNC-7 guidelines to identify prehypertensives in whom ABPM was then assessed. Fasting plasma samples were assayed for inflammatory markers. Brachial artery flow-mediated dilation (FMD) at rest and during reactive hyperemia was measured in a subset of prehypertensives.
  
  
  RESULTS
  Subjects in the masked-hypertension sub-group had a higher hsCRP (P = 0.04) and diminished endothelial function (P = 0.03) compared to the true-prehypertensive sub-group (office-BP: 120/80-139/89 mm Hg and ABPM: daytime <135/85 mm Hg or night-time <120/70 mm Hg). Regression analysis showed that endothelial function was inversely related to hsCRP amongst the masked-hypertensive sub-group (R(2) = 0.160; P = 0.04).
  
  
  CONCLUSIONS
  Masked-hypertension was identified in 58% of African Americans which suggests that a masking phenomenon may exist in a sub-group of prehypertensives who also seem to have a diminished endothelial function that could be mediated by an elevated subclinical inflammation leading to the increased CV disease.
authors.affiliation: Hypertension, Molecular and Applied Physiology Laboratory, Department of Kinesiology, Temple University, Philadelphia, Pennsylvania, USA. praveenv@temple.edu
authors.forename: Praveen
authors.initials: P
authors.lastname: Veerabhadrappa
authors.forename: Keith M
authors.initials: KM
authors.lastname: Diaz
authors.forename: Deborah L
authors.initials: DL
authors.lastname: Feairheller
authors.forename: Katie M
authors.initials: KM
authors.lastname: Sturgeon
authors.forename: Sheara T
authors.initials: ST
authors.lastname: Williamson
authors.forename: Deborah L
authors.initials: DL
authors.lastname: Crabbe
authors.forename: Abul M
authors.initials: AM
authors.lastname: Kashem
authors.forename: Michael D
authors.initials: MD
authors.lastname: Brown
mesh_terms: D000328:Adult; D001741:Black or African American; D000368:Aged; D018660:Blood Pressure Monitoring, Ambulatory; D002097:C-Reactive Protein / Q000032:analysis; D004730:Endothelium, Vascular / Q000502:physiology*; D005260:Female; D006801:Humans; D007958:Leukocyte Count; D008297:Male; D059468:Masked Hypertension / Q000503:physiopathology*; D008875:Middle Aged; D009569:Nitric Oxide / Q000502:physiology; D058246:Prehypertension / Q000503:physiopathology; D012039:Regional Blood Flow; D014664:Vasodilation
chemical_list: D009569:Nitric Oxide; D002097:C-Reactive Protein