Contribution of Circulating Angiotensinogen Concentrations to Variations in Aldosterone and Blood Pressure in a Group of African Ancestry Depends on Salt Intake
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.
- Received August 15, 2011.
- Revision received September 2, 2011.
- Accepted October 31, 2011.
- © 2011 American Heart Association, Inc.