title: Hemodynamic and hormonal patterns of untreated essential hypertension in men and women.
abstract: BACKGROUND
  Knowledge of hemodynamic factors accounting for the development of hypertension should help to tailor therapeutic approaches and improve blood pressure control. Few data exist regarding sex differences of hemodynamic factors contributing to hypertension progression among patients with untreated nondiabetic stage I and II prehypertension (PreHyp) as defined by the Joint National Committee-7 guidelines (JNC-7).
  
  
  METHODS
  We utilized noninvasive impedance cardiography, applanation tonometry and plasma measures of angiotensin II, angiotensin (1-7), serum aldosterone, high-sensitivity C-reactive protein (hs-CRP) and cytokine biomarkers of inflammation to characterize the hemodynamic and hormonal profile of 100 patients with untreated hypertension (39 women).
  
  
  RESULTS
  Despite there being no differences between women and men in terms of office blood pressure, heart rate and body mass index, men demonstrated lower values of pulse pressure, systemic vascular resistance, brachial artery pulse wave velocity and augmentation index. In each of the three hypertension categories, the increased blood pressure in men was associated with significant augmentations in stroke volume and cardiac output compared with women. Sex-related hemodynamic differences were associated in women with higher plasma levels of leptin, hs-CRP, plasma angiotensin II and serum aldosterone, and no differences in the serum concentrations of cytokinins. In women but not men, hs-CRP correlated with plasma concentrations of transforming growth factor β1 (TGFβ1) and body weight; in addition, plasma TGFβ1 correlated with levels of serum vascular cell adhesion molecule 1.
  
  
  CONCLUSIONS
  The impact of sex differences in the hemodynamic factors accounting for the elevation in arterial pressure in subjects with essential hypertension has been poorly characterized or this information is not available. We suggest that this gap in knowledge may adversely influence choices of drug treatment since our study shows for the first time significant differences in the hemodynamic and hormonal mechanisms accounting for the increased blood pressure in women compared to men.
authors.affiliation: Laboratory of Translational Hypertension Research, Department of Surgery, Wake Forest University School of Medicine, Winston Salem, NC 27157, USA.
authors.forename: Carlos M
authors.initials: CM
authors.lastname: Ferrario
authors.forename: Jewell A
authors.initials: JA
authors.lastname: Jessup
authors.forename: Ronald D
authors.initials: RD
authors.lastname: Smith
mesh_terms: D015415:Biomarkers / Q000097:blood; D002307:Cardiography, Impedance; D005260:Female; D006439:Hemodynamics; D006728:Hormones / Q000097:blood*; D006801:Humans; D006973:Hypertension / Q000097:blood* / Q000175:diagnosis / Q000503:physiopathology*; D018836:Inflammation Mediators / Q000097:blood; D008297:Male; D008365:Manometry; D008875:Middle Aged; D058246:Prehypertension / Q000097:blood / Q000175:diagnosis / Q000503:physiopathology; D011379:Prognosis; D012084:Renin-Angiotensin System; D012737:Sex Factors
chemical_list: D015415:Biomarkers; D006728:Hormones; D018836:Inflammation Mediators
keywords: angiotensin II; blood pressure; cardiac output; central aortic pressure; essential hypertension; inflammation; vascular disease