title: Association of urinary N-domain Angiotensin I-converting enzyme with plasma inflammatory markers and endothelial function.
abstract: The aim of this study was to investigate the association between urinary 90 kDa N-domain Angiotensin I-converting enzyme (ACE) form with C-reactive protein (CRP) and homocysteine plasma levels (Hcy), urinary nitric oxide (NOu), and endothelial function (EF) in normotensive subjects. Forty healthy subjects were evaluated through brachial Doppler US to test the response to reactive hyperemia and a panel of blood tests to determine CRP and Hcy levels, NOu, and urinary ACE. They were divided into groups according to the presence (ACE90+) or absence (ACE90-) of the 90 kDa ACE, the presence (FH+) or absence (FH-) of family history of hypertension, and the presence or absence of these two variables FH+/ACE90+ and FH-/ACE90-. We found an impaired endothelial dilatation in subjects who presented the 90 kDa N-domain ACE as follows: 11.4% +/- 5.3% in ACE90+ compared with 17.6% +/- 7.1% in ACE90- group and 12.4% +/- 5.6% in FH+/ACE90+ compared with 17.7% +/- 6.2% in FH-/ACE90- group, P < 0.05. Hcy and CRP levels were statistically significantly lower in FH+/ACE90+ than in FH-/ACE90- group, as follows: 10.0 +/- 2.3 microM compared with 12.7 +/- 1.5 microM, and 1.3 +/- 1.8 mg/L compared with 3.6 +/- 2.0 mg/L, respectively. A correlation between flow-mediated dilatation (FMD) and CRP, Hcy, and NOu levels was not found. Our study suggests a reduction in the basal NO production confirmed by NOu analysis in subjects with the 90 kDa N-domain ACE isoform alone or associated with a family history of hypertension. Our data suggest that the presence of the 90 kDa N-domain ACE itself may have a negative impact on flow-mediated dilatation stimulated by reactive hyperemia.
authors.affiliation: Department of Medicine, Nephrology Division, Federal University of São Paulo, São Paulo, Brazil.
authors.forename: Fernanda B
authors.initials: FB
authors.lastname: Fernandes
authors.forename: Frida L
authors.initials: FL
authors.lastname: Plavnik
authors.forename: Andressa Ms
authors.initials: AM
authors.lastname: Teixeira
authors.forename: Dejaldo Mj
authors.initials: DM
authors.lastname: Christofalo
authors.forename: Sergio A
authors.initials: SA
authors.lastname: Ajzen
authors.forename: Elisa Ms
authors.initials: EM
authors.lastname: Higa
authors.forename: Fernanda A
authors.initials: FA
authors.lastname: Ronchi
authors.forename: Ricardo Cc
authors.initials: RC
authors.lastname: Sesso
authors.forename: Dulce E
authors.initials: DE
authors.lastname: Casarini
mesh_terms: D000293:Adolescent; D000328:Adult; D050197:Atherosclerosis / Q000097:blood / Q000503:physiopathology / Q000652:urine; D015415:Biomarkers / Q000097:blood*; D002097:C-Reactive Protein / Q000032:analysis; D003430:Cross-Sectional Studies; D004730:Endothelium, Vascular / Q000502:physiology*; D005192:Family Health; D006710:Homocysteine / Q000097:blood; D006801:Humans; D006973:Hypertension / Q000097:blood / Q000503:physiopathology / Q000652:urine; D007249:Inflammation / Q000097:blood* / Q000503:physiopathology; D008297:Male; D007703:Peptidyl-Dipeptidase A / Q000652:urine*; D017434:Protein Structure, Tertiary; D014664:Vasodilation / Q000502:physiology
chemical_list: D015415:Biomarkers; D006710:Homocysteine; D002097:C-Reactive Protein; D007703:Peptidyl-Dipeptidase A