Commonwealth Scientific and Industrial Research Organisation, Animal, Food and Health Science, Adelaide, South Australia, Australia; Discipline of Physiology, Faculty of Health Science, University of Adelaide, South Australia, Australia; The National Health and Medical Research Council of Australia Centre of Clinical Research Excellence in Nutritional Physiology, Interventions and Outcomes, Adelaide, South Australia, Australia.
Discipline of Physiology, Faculty of Health Science, University of Adelaide, South Australia, Australia; The National Health and Medical Research Council of Australia Centre of Clinical Research Excellence in Nutritional Physiology, Interventions and Outcomes, Adelaide, South Australia, Australia; School of Pharmacy and Medical Sciences, Division of Health Sciences, University of South Australia, Adelaide, South Australia 5000, Australia.
Atherosclerosis. 2014 Jan;232(1):211-6. doi: 10.1016/j.atherosclerosis.2013.10.032. Epub 2013 Nov 20.
The aim of the study was to determine if a high salt meal containing 65 mmol Na causes a rise in sodium concentrations and a reduction in plasma nitrate/nitrite concentrations (an index of nitric oxide production). Secondary aims were to determine the effects of a high salt meal on augmentation index (AIx) a measure of arterial stiffness and markers of endothelial function.
In a randomised cross-over study 16 healthy normotensive adults consumed a low sodium soup containing 5 mmol Na and a high sodium soup containing 65 mmol Na. Sodium, plasma nitrate/nitrite, endothelin-1 (ET-1), C-reactive protein (CRP), vasopressin (AVP) and atrial natriuretic peptide (ANP) concentrations before and every 30 min after the soup for 2 h. Blood pressure (BP) and AI were also measured at these time points. There were significant increases in serum sodium, osmolality and chloride in response to the high sodium meal. However plasma nitrate/nitrite concentrations were not different between meals (meal p = 0.812; time p = 0.45; meal × time interaction p = 0.50). Plasma ANP, AVP and ET-1 were not different between meals. AI was significantly increased following the high sodium meal (p = 0.02) but there was no effect on BP.
A meal containing 65 mmol Na increases serum sodium and arterial stiffness but does not alter postprandial nitrate/nitrite concentration in healthy normotensive individuals. Further research is needed to explore the mechanism by which salt affects vascular function in the postprandial period. This trial was registered with the Australian and New Zealand Clinical Trials Registry Unique Identifier: ACTRN12611000583943http://www.anzctr.org.au/trial_view.aspx?ID=343019.
本研究旨在确定高盐餐（含 65mmol Na）是否会引起钠离子浓度升高和血浆硝酸盐/亚硝酸盐浓度降低（一氧化氮生成的指标）。次要目的是确定高盐餐对动脉僵硬的指标增强指数（AIx）和内皮功能标志物的影响。
在一项随机交叉研究中，16 名健康的血压正常成年人分别食用含 5mmol Na 的低钠汤和含 65mmol Na 的高钠汤。在 2 小时内，分别在汤前和汤后每 30 分钟测量一次血清钠、血浆硝酸盐/亚硝酸盐、内皮素-1（ET-1）、C 反应蛋白（CRP）、血管加压素（AVP）和心房利钠肽（ANP）浓度。在这些时间点还测量了血压（BP）和 AI。高盐餐引起血清钠、渗透压和氯显著升高。然而，两餐之间血浆硝酸盐/亚硝酸盐浓度无差异（餐 p=0.812；时间 p=0.45；餐×时间交互作用 p=0.50）。两餐之间血浆 ANP、AVP 和 ET-1 无差异。高盐餐后 AI 显著升高（p=0.02），但对 BP 无影响。
含 65mmol Na 的膳食会增加血清钠和动脉僵硬，但不会改变健康血压正常个体餐后硝酸盐/亚硝酸盐浓度。需要进一步研究盐在后餐期间影响血管功能的机制。该试验在澳大利亚和新西兰临床试验注册中心注册，唯一标识符：ACTRN12611000583943http://www.anzctr.org.au/trial_view.aspx？ID=343019。
