title: Racial differences in the relation between blood pressure and insulin resistance.
abstract: BACKGROUND
  Insulin resistance and the concomitant compensatory hyperinsulinemia have been implicated in the pathogenesis of hypertension. However, reports on the relation between insulin and blood pressure are inconsistent. This study was designed to investigate the possibility of racial differences in this relation.
  
  
  METHODS
  We studied 116 Pima Indians, 53 whites, and 42 blacks who were normotensive and did not have diabetes; the groups were comparable with respect to mean age (29, 30, and 31 years, respectively) and blood pressure (113/70, 111/68, and 113/68 mm Hg, respectively). Insulin resistance was determined by the euglycemic-hyperinsulinemic clamp technique during low-dose (40 mU per square meter of body-surface area per minute) and high-dose (400 mU per square meter per minute) insulin infusions.
  
  
  RESULTS
  The Pima Indians had higher fasting plasma insulin concentrations than the whites or blacks (176, 138, and 122 pmol per liter, respectively; P = 0.002) and lower rates of whole-body glucose disposal during both the low-dose (12.7, 17.1, and 19.5 mmol per minute; P less than 0.001) and the high-dose (38.0, 43.1, and 45.7 mmol per minute; P less than 0.001) insulin infusions. After adjustment for age, sex, body weight, and percentage of body fat, mean blood pressure (calculated as 1/3 systolic pressure + 2/3 diastolic pressure) was significantly correlated with the fasting plasma insulin concentration (r = 0.42) and the rate of glucose disposal during the low-dose (r = -0.41) and high-dose (r = -0.49) insulin infusions (P less than 0.01 for each) in whites, but not in Pima Indians (r = -0.06, -0.02, and -0.04, respectively) or blacks (r = -0.10, -0.04, and 0.02, respectively).
  
  
  CONCLUSIONS
  The relations between insulinemia, insulin resistance, and blood pressure differ among racial groups and may be mediated by mechanisms active in whites, but not in Pima Indians or blacks.
authors.affiliation: Phoenix Epidemiology and Clinical Research Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Ariz.
authors.forename: M F
authors.initials: MF
authors.lastname: Saad
authors.forename: S
authors.initials: S
authors.lastname: Lillioja
authors.forename: B L
authors.initials: BL
authors.lastname: Nyomba
authors.forename: C
authors.initials: C
authors.lastname: Castillo
authors.forename: R
authors.initials: R
authors.lastname: Ferraro
authors.forename: M
authors.initials: M
authors.lastname: De Gregorio
authors.forename: E
authors.initials: E
authors.lastname: Ravussin
authors.forename: W C
authors.initials: WC
authors.lastname: Knowler
authors.forename: P H
authors.initials: PH
authors.lastname: Bennett
authors.forename: B V
authors.initials: BV
authors.lastname: Howard
mesh_terms: D000328:Adult; D000704:Analysis of Variance; D001130:Arizona; D044383:Black People; D001794:Blood Pressure / Q000235:genetics*; D004734:Energy Metabolism; D005260:Female; D006801:Humans; D007198:Indians, North American; D007328:Insulin / Q000097:blood*; D007333:Insulin Resistance / Q000235:genetics*; D008297:Male; D044469:Racial Groups; D014481:United States; D044465:White People; D001741:Black or African American
chemical_list: D007328:Insulin