title: Elevated VEGF-plasma levels in young patients with mild essential hypertension.
abstract: BACKGROUND
  Growing evidence shows that inflammation plays a pivotal role in the pathophysiology of essential hypertension (EH). Vascular endothelial cell growth factor (VEGF) is currently discussed as a possible mediator of inflammation. To investigate the hypothesis that VEGF plays a role as an inflammatory mediator in EH we performed the present pilot study of young patients in a very early stage of EH.
  
  
  METHODS
  15 young patients with mild EH [33.8 +/- 7.3 years, systolic blood pressure (SBP): 143.8 +/- 10.5 mmHg, diastolic blood pressure (DBP): 88.2 +/- 11.1 mmHg, mean arterial pressure (MAP) 106.6 +/- 10.4 mmHg] and 15 healthy controls (31.7 +/- 10.6 years) were examined. Blood was drawn from a peripheral vein and serum levels of VEGF, monocyte-chemoattractant-protein (MCP)-1, high-sensitivity C-reactive protein (hsCRP), interleukin (IL)-6, and tumour-necrosis-factor (TNF)-alpha were measured via commercially available enzyme-linked immunoassays.
  
  
  RESULTS
  Hypertensives showed increased plasma levels of VEGF (P < 0.05) and MCP-1 (P < 0.05). VEGF positively correlated with MAP (r = 0.46, P < 0.05) and MCP-1 (r = 0.63, P < 0.01). Multivariate analysis demonstrated VEGF to be an independent predictor of MCP-1 levels. Furthermore, hypertensives had higher levels of hsCRP (P < 0.01), IL-6 (P < 0.001) and TNF-alpha (P < 0.05). IL-6 levels correlated with SBP (r = 0.59, P < 0.001), DBP (r = 0.67, P < 0.001) and MAP (r = 0.46, P < 0.001). A significant positive correlation was also found between hsCRP levels and SBP (r = 0.39, P < 0.05).
  
  
  CONCLUSIONS
  This pilot study demonstrates that in an early state of EH, inflammatory pathways have already been activated. Besides classical pro-inflammatory cytokines, VEGF serum levels are significantly elevated. The positive correlation of VEGF with MCP-1 is suggestive for the already described induction of MCP-1 via VEGF.
authors.affiliation: Department of Cardiology, University of Erlangen-Nuremberg, Erlangen, Germany. ch.stumpf@web.de
authors.forename: C
authors.initials: C
authors.lastname: Stumpf
authors.forename: J
authors.initials: J
authors.lastname: Jukic
authors.forename: A
authors.initials: A
authors.lastname: Yilmaz
authors.forename: D
authors.initials: D
authors.lastname: Raaz
authors.forename: R E
authors.initials: RE
authors.lastname: Schmieder
authors.forename: W G
authors.initials: WG
authors.lastname: Daniel
authors.forename: C D
authors.initials: CD
authors.lastname: Garlichs
mesh_terms: D000328:Adult; D001794:Blood Pressure / Q000502:physiology*; D016022:Case-Control Studies; D005260:Female; D006801:Humans; D006973:Hypertension / Q000097:blood* / Q000503:physiopathology; D018836:Inflammation Mediators / Q000097:blood / Q000378:metabolism*; D008297:Male; D010865:Pilot Projects; D042461:Vascular Endothelial Growth Factor A / Q000097:blood / Q000378:metabolism*; D055815:Young Adult
chemical_list: D018836:Inflammation Mediators; D042461:Vascular Endothelial Growth Factor A