title: Gender-specific association of the plasminogen activator inhibitor-1 4G/5G polymorphism with central arterial blood pressure.
abstract: BACKGROUND
  The functional plasminogen activator inhibitor-1 (PAI-1) 4G/5G polymorphism has previously been associated with hypertension. In recent years, central blood pressure, rather than brachial has been argued a better measure of cardiovascular damage and clinical outcome. The aim of this study was to investigate the possible influence of the 4G/5G polymorphism on central arterial blood pressure in a cohort of elderly individuals.
  
  
  METHODS
  We studied 410 individuals, 216 men and 194 women, aged 70-88. Central pressures and pulse waveforms were calculated from the radial artery pressure waveform by the use of the SphygmoCor system and a generalized transfer function. Brachial pressure was recorded using oscillometric technique (Dinamap, Critikon, Tampa, FL). PAI-1 antigen was determined in plasma.
  
  
  RESULTS
  The results showed that central pressures were higher in women carrying the PAI-1 4G/4G genotype compared to female carriers of the 5G/5G genotype, (P = 0.025, P = 0.002, and P = 0.002 for central systolic-, diastolic-, and mean arterial pressure, respectively). The association remained after adjustment for potentially confounding factors related to hypertension. No association of the PAI-1 genotype with blood pressure was found in men. Multiple regression analysis revealed an association between PAI-1 genotype and plasma PAI-1 levels (P = 0.048).
  
  
  CONCLUSIONS
  Our findings show a gender-specific association of the PAI-1 4G/5G polymorphism with central arterial blood pressure. The genotype effect was independent of other risk factors related to hypertension, suggesting that impaired fibrinolytic potential may play an important role in the development of central hypertension in women.
authors.affiliation: Division of Cardiovascular Medicine, Department of Medical and Health Sciences, Faculty of Health Sciences, Linköping University, Linköping, Sweden. hanna.bjorck@liu.se
authors.forename: Hanna M
authors.initials: HM
authors.lastname: Björck
authors.forename: Per
authors.initials: P
authors.lastname: Eriksson
authors.forename: Urban
authors.initials: U
authors.lastname: Alehagen
authors.forename: Rachel
authors.initials: R
authors.lastname: De Basso
authors.forename: Liza U
authors.initials: LU
authors.lastname: Ljungberg
authors.forename: Karin
authors.initials: K
authors.lastname: Persson
authors.forename: Ulf
authors.initials: U
authors.lastname: Dahlström
authors.forename: Toste
authors.initials: T
authors.lastname: Länne
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D001794:Blood Pressure / Q000235:genetics* / Q000502:physiology; D015331:Cohort Studies; D005260:Female; D005500:Follow-Up Studies; D020022:Genetic Predisposition to Disease / Q000235:genetics; D005838:Genotype; D006801:Humans; D006973:Hypertension / Q000453:epidemiology / Q000235:genetics / Q000503:physiopathology; D008297:Male; D017395:Plasminogen Activator Inhibitor 1 / Q000235:genetics*; D011110:Polymorphism, Genetic / Q000235:genetics*; D012307:Risk Factors; D012727:Sex Characteristics; D013548:Sweden
chemical_list: D017395:Plasminogen Activator Inhibitor 1