Journal
AMERICAN JOURNAL OF HYPERTENSION
Volume 28, Issue 2, Pages 208-215Publisher
OXFORD UNIV PRESS
DOI: 10.1093/ajh/hpu115
Keywords
aldosterone; blood pressure; epidemiology; hypertension; relative aldosterone excess; renin; salt intake
Categories
Funding
- Ministry of Education, Culture, Sports, Science, and Technology, Japan [23249036, 23390171, 24390084, 24591060, 24790654, 25461205, 25461083, 25860156, 25253059, 26860093, 26282200]
- Intramural Research Fund for Cardiovascular Diseases of National Cerebral and Cardiovascular Center [22-4-5]
- Grants-in-Aid for Scientific Research [25253059, 13J09328, 26860093, 24790654, 24591060, 25461083, 26282200, 25293193, 25860156, 25461205] Funding Source: KAKEN
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BACKGROUND In cross-sectional studies, the aldosterone-to-renin ratio (ARR) has been reported to be associated with hypertension under conditions of higher sodium intake. The objective of this prospective study was to investigate the association between ARR and the development of hypertension in community residents stratified by dietary sodium intake. METHODS From the general population of Ohasama, we obtained plasma renin activity (PRA) and plasma aldosterone concentrations (PACs) for 608 participants (mean age = 57.6 years; 71.4% women) without hypertension at baseline. Using the Cox model, we computed the adjusted hazard ratio (HR) of natural log-transformed ARR (lnARR) for the development of hypertension, defined as blood pressure >= 140/90 mm Hg or start of treatment with antihypertensive drugs during follow-up. RESULTS During a mean follow-up of 6.8 years, 298 participants developed hypertension. The median PRA, PAC, and ARR were 1.2 ng/ml/hour, 6.6 ng/dl, and 5.5 ng/dl per ng/ml/hour, respectively. Each 1 SD increase in lnARR was associated with an increased risk for the development of hypertension in participants overall (HR = 1.18; P = 0.007). In participants with higher sodium intake (median >= 4,102 mg/day), a significant association of lnARR with hypertension remained (HR = 1.25; P = 0.009), whereas no significant association was observed in participants with lower sodium intake (P = 0.18). Participants who developed hypertension had significantly lower PRA than those who did not (P = 0.003), despite no differences in PAC (P = 0.91). CONCLUSIONS These results raise the hypothesis that relative aldosterone excess may have a deleterious effect on the development of hypertension by contributing to salt/volume-related hypertension.
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