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. © 2011 American Heart Association, Inc.