Association of aldosterone-to-renin ratio with hypertension differs by sodium intake: the Ohasama study.
Association of aldosterone-to-renin ratio with hypertension differs by sodium intake: the Ohasama study.
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醛固酮/肾素比率与高血压的关联因钠摄入量而异:Ohasama 研究。
DOI:
10.1093/ajh/hpu115
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发表时间:
2015
期刊:
影响因子:
--
通讯作者:
et al.
中科院分区:
文献类型:
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作者:
Satoh M;Kikuya M;Hosaka M;et al.
BACKGROUNDIn 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.METHODSFrom 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 ≥140/90mm Hg or start of treatment with antihypertensive drugs during follow-up.RESULTSDuring a mean follow-up of 6.8 years, 298 participants developed hypertension. The median PRA, PAC, and ARR were 1.2ng/ml/hour, 6.6ng/dl, and 5.5ng/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 ≥4,102mg/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).CONCLUSIONSThese 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.