Intensive Care Unit and Department of Cardiology, Toranomon Hospital, Tokyo 105-8470, Japan.
Cardiovascular Center, St. Luke's International Hospital, Tokyo 104-8560, Japan.
Nutrients. 2020 May 14;12(5):1422. doi: 10.3390/nu12051422.
The potential contribution of serum osmolarity in the modulation of blood pressure has not been evaluated. This study was done to examine the relationship between hyperosmolarity and hypertension in a five-year longitudinal design. We enrolled 10,157 normotensive subjects without diabetes who developed hypertension subsequently as determined by annual medical examination in St. Luke's International Hospital, Tokyo, between 2004 and 2009. High salt intake was defined as >12 g/day by a self-answered questionnaire and hyperosmolarity was defined as >293 mOsm/L serum osmolarity, calculated using serum sodium, fasting blood glucose, and blood urea nitrogen. Statistical analyses included adjustments for age, gender, body mass index, smoking, drinking alcohol, dyslipidemia, hyperuricemia, and chronic kidney disease. In the patients with normal osmolarity, the group with high salt intake had a higher cumulative incidence of hypertension than the group with normal salt intake (8.4% versus 6.7%, = 0.023). In contrast, in the patients with high osmolarity, the cumulative incidence of hypertension was similar in the group with high salt intake and in the group with normal salt intake (13.1% versus 12.9%, = 0.84). The patients with hyperosmolarity had a higher incidence of hypertension over five years compared to that of the normal osmolarity group ( < 0.001). After multiple adjustments, elevated osmolarity was an independent risk for developing hypertension (OR (odds ratio), 1.025; 95% CI (confidence interval), 1.006-1.044), regardless of the amount of salt intake. When analyzed in relation to each element of calculated osmolarity, serum sodium and fasting blood glucose were independent risks for developing hypertension. Our results suggest that hyperosmolarity is a risk for developing hypertension regardless of salt intake.
血清渗透压在调节血压方面的潜在作用尚未得到评估。本研究采用 5 年纵向设计,旨在探讨高渗透压与高血压之间的关系。我们纳入了 2004 年至 2009 年期间在东京圣卢克国际医院接受年度体检的 10157 例无糖尿病的血压正常的受试者,这些受试者随后被诊断为高血压。高盐摄入量通过自我回答问卷定义为 >12 g/天,高渗透压定义为血清渗透压 >293 mOsm/L,通过血清钠、空腹血糖和血尿素氮计算得出。统计学分析包括对年龄、性别、体重指数、吸烟、饮酒、血脂异常、高尿酸血症和慢性肾脏病进行调整。在渗透压正常的患者中,高盐摄入组的高血压累积发生率高于低盐摄入组(8.4%比 6.7%,= 0.023)。相比之下,在高渗透压患者中,高盐摄入组和低盐摄入组的高血压累积发生率相似(13.1%比 12.9%,= 0.84)。高渗透压患者在 5 年内发生高血压的发生率高于渗透压正常组(<0.001)。经过多次调整,渗透压升高是高血压发生的独立危险因素(OR,1.025;95%CI,1.006-1.044),与盐摄入量无关。当按渗透压计算的每个元素进行分析时,血清钠和空腹血糖是高血压发生的独立危险因素。我们的研究结果表明,高渗透压是高血压的危险因素,与盐摄入量无关。