title: Hypertension and triglyceride catabolism: implications for the hemodynamic model of the metabolic syndrome.
abstract: OBJECTIVE
  We sought to determine if hypertensive adults have a blunted triglyceride catabolic rate (TG K(2)) and if related hemodynamic and vascular alterations are determinants of TG K(2).
  
  
  METHODS
  Fasting levels of insulin, glucose, lipoproteins and plasma catecholamines were measured in 10 normotensive and 10 hypertensive adults. TG K(2) was determined by an intravenous fat tolerance test. Forearm blood flow, maximum forearm blood flow and minimal forearm vascular resistance were determined by strain gauge plethysmography. Vascular compliance and systemic hemodynamics were measured by computerized arterial pulse waveform analysis.
  
  
  RESULTS
  Compared to normotensives, hypertensives had a significantly elevated blood pressure (145 +/- 8/94 +/- 11 versus 111 +/- 15/74 +/- 14 mm Hg, p < 0.001), systemic vascular resistance (1695 +/- 441 versus 1172 +/- 430 dynes x sec x cm(-5), p = 0.02) and reduced large vessel compliance (11.7 +/- 3.6 versus 15.1 +/- 3.1 ml/mm Hg x 100, p = 0.04). There were no significant group differences in TG K(2) (3.07 +/- 2.01 versus 2.88 +/- 2.12 mg/dL/min, p = 0.85) or other metabolic and anthropometric variables. TG K(2) was not predicted by the forearm vascular measures or the hemodynamic variables, but was correlated to waist/hip ratio (r = -0.71, p = 0.001), fasting triglycerides (r = -0.64, p = 0.003), and male gender (r = 0.56, p = 0.012). An enhanced TG K(2) was independently predicted by a reduced small vessel compliance (r = -0.61, p = 0.006).
  
  
  CONCLUSIONS
  Elevated blood pressure per se and hypertension-related hemodynamic and vascular alterations are not associated with reduced TG K(2) or other metabolic abnormalities. Rather, aspects of the insulin resistance syndrome are closely related to abdominal adiposity. The independent association between small vessel compliance and TG K(2) deserves further investigation.
authors.affiliation: Division of Hypertension, University of Michigan, 3918 Taubman Center, 1500 East Medical Center Drive, Ann Arbor, MI 48104, USA. Robdbrok@groupwise.umich.edu
authors.forename: Robert D
authors.initials: RD
authors.lastname: Brook
authors.forename: Lynn
authors.initials: L
authors.lastname: Glazewski
authors.forename: Sanjay
authors.initials: S
authors.lastname: Rajagopalan
authors.forename: Robert L
authors.initials: RL
authors.lastname: Bard
mesh_terms: D000328:Adult; D001794:Blood Pressure / Q000502:physiology; D001808:Blood Vessels / Q000503:physiopathology*; D016022:Case-Control Studies; D005260:Female; D006439:Hemodynamics / Q000502:physiology*; D006801:Humans; D006973:Hypertension / Q000378:metabolism*; D007333:Insulin Resistance / Q000502:physiology; D008297:Male; D024821:Metabolic Syndrome / Q000378:metabolism / Q000503:physiopathology*; D010991:Plethysmography; D014280:Triglycerides / Q000378:metabolism*
chemical_list: D014280:Triglycerides