Sex influences the cardiorenal risk associated with body mass index (BMI). The role of the renin–angiotensin–aldosterone system in adiposity-mediated cardiorenal risk profiles in healthy, non-obese men and women was investigated.


Systemic and renal hemodynamic responses to angiotensin-II (AngII) as a function of BMI, waist and hip circumference, waist–hip ratio, as well as fat and lean mass were measured in 18 men and 25 women in high-salt balance, stratified by BMI (<25 kg/m2 (ideal body weight (IBW)) vs. ≥25 kg/m2 overweight)).


In men (n = 7, BMI 23 ± 1 kg/m2) and women (n = 14, BMI 22 ± 2 kg/m2) of IBW, BMI was not associated with the systolic blood pressure (SBP) response to AngII. In contrast, overweight men (n = 11, 29 ± 2 kg/m2) demonstrated a progressively more blunted vasoconstrictor SBP response to AngII challenge as BMI increased (P = 0.007), even after adjustment for covariates. Women maintained the same relationship between BMI and the SBP response to AngII irrespective of weight status (P = 0.2, IBW vs. overweight women). Compared to BMI, other adiposity measures showed similar associations to systemic AngII responsiveness in men but not in women. Increasing BMI was associated with a blunted renovasoconstrictor response to AngII in all subjects, but was more pronounced in men.


Sex influences the effect of adiposity on vascular angiotensin-responsiveness.