title: Contribution of circulating angiotensinogen concentrations to variations in aldosterone and blood pressure in a group of African ancestry depends on salt intake.
abstract: In high-Na(+), low-K(+) diets, which suppress renin release in salt-sensitive groups, the mechanisms maintaining increases in renin-angiotensin-aldosterone system activation downstream from renin and renin-angiotensin-aldosterone system-induced effects on blood pressure (BP) are uncertain. Whether circulating angiotensinogen concentrations (AGT) or its determinants may contribute to maintaining serum aldosterone concentrations (aldosterone) and increases in BP on high-Na(+), low-K(+) diets was evaluated in 579 participants of a community sample of African ancestry. Plasma renin concentrations were inversely related to BP (P<0.0001) and an index of salt intake (24-hour urinary Na(+)/K(+), P<0.0001). An interaction between AGT and urinary Na(+)/K(+) was independently associated with aldosterone (P<0.001) and systolic BP (SBP; P<0.05). Independent of confounders, in participants with urinary Na(+)/K(+) at or more than the median for the sample, AGT was positively associated with aldosterone (P<0.0001) and SBP (P<0.005). No independent AGT-aldosterone or AGT-SBP relationships were noted in participants with urinary Na(+)/K(+) less than the median for the sample. Standardized β-coefficients (slopes) of AGT-aldosterone and AGT-SBP relationships were greater in participants with urinary Na(+)/K(+) at or more than the median (AGT-aldosterone=0.30±0.06, AGT-SBP=0.16±0.05) compared with those with urinary Na(+)/K(+) less than the median (AGT-aldosterone=-0.04±0.06; AGT-SBP=-0.03±0.05; P<0.01-0.0001 for comparison of slopes). The AGT-SBP relationship in participants with urinary Na(+)/K(+) at or more than the median for the sample was equivalent to the relationship between body mass index and BP. In conclusion, in participants of African ancestry, in the presence of high-Na(+), low-K(+) diets, which suppress renin release, renin-angiotensin-aldosterone system activation and its impact on BP are maintained in part by AGT.
authors.affiliation: Cardiovascular Pathophysiology and Genomics Research Unit, School of Physiology, University of the Witwatersrand Medical School, 7 York Rd, Parktown, 2193 Johannesburg, South Africa.
authors.forename: Frederic S
authors.initials: FS
authors.lastname: Michel
authors.forename: Gavin R
authors.initials: GR
authors.lastname: Norton
authors.forename: Olebogeng H I
authors.initials: OH
authors.lastname: Majane
authors.forename: Margaret
authors.initials: M
authors.lastname: Badenhorst
authors.forename: Leanda
authors.initials: L
authors.lastname: Vengethasamy
authors.forename: Janice
authors.initials: J
authors.lastname: Paiker
authors.forename: Muzi J
authors.initials: MJ
authors.lastname: Maseko
authors.forename: Pinhas
authors.initials: P
authors.lastname: Sareli
authors.forename: Angela J
authors.initials: AJ
authors.lastname: Woodiwiss
mesh_terms: D000328:Adult; D001741:Black or African American / Q000706:statistics & numerical data*; D000450:Aldosterone / Q000097:blood*; D000808:Angiotensinogen / Q000097:blood* / Q000235:genetics; D001794:Blood Pressure / Q000502:physiology*; D002097:C-Reactive Protein / Q000378:metabolism; D003404:Creatinine / Q000652:urine; D005260:Female; D005838:Genotype; D006801:Humans; D006977:Hypertension, Renal / Q000208:ethnology* / Q000235:genetics / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D017419:Potassium, Dietary / Q000008:administration & dosage / Q000652:urine; D012083:Renin / Q000097:blood; D012084:Renin-Angiotensin System / Q000502:physiology; D012307:Risk Factors; D017673:Sodium Chloride, Dietary / Q000008:administration & dosage* / Q000652:urine; D055815:Young Adult
chemical_list: D017419:Potassium, Dietary; D017673:Sodium Chloride, Dietary; D000808:Angiotensinogen; D000450:Aldosterone; D002097:C-Reactive Protein; D003404:Creatinine; D012083:Renin