Abstract

It is established that men have higher blood pressures than women and that African Americans (AA) have an increased likelihood of developing hypertension and renal disease compared to their Caucasian (CN) counterparts. However, the mechanism(s) accounting for these differences remain to be established. In the present study, we assessed mean arterial pressures (MAP), as well as ACE and ACE2 that form and metabolize Angiotensin (Ang) II, the primary effector peptide of the renin angiotensin system (RAS), in urine from AA male (n=8), AA female (n=9) and CN female (n=4) adolescents at 14 years of age. MAP did not differ significantly between groups [AA males: 74±2 mmHg; AA females: 76±1mmHg; CN females: 73±1mmHg]. ACE activity was lower in AA females [0.7±0.2 fmol/min/g creatinine] than AA males [1.3±0.2 fmol/min/g creatinine; p<0.05], but did not differ from CN females [0.8±0.3 fmol/min/g creatinine]. Conversely, ACE2 activity was lower in AA females [0.9±0.2 fmol/min/g creatinine] compared to CN females [1.7±0.4 fmol/min/g creatinine; p<0.05] but not in AA males [1.0±0.3 fmol/min/g creatinine]. These findings suggest that sex and racial differences in urinary ACE and ACE2 activities are evident in young adults in the absence of changes in blood pressure. We speculate that lower ACE2 activity may contribute to the development of cardiovascular disease particularly in AA females. HD047584‐S3; HL‐56973; M01‐RR07122

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