Short-term high salt intake reduces brachial artery and microvascular function in the absence of changes in blood pressure.
Short-term high salt intake reduces brachial artery and microvascular function in the absence of changes in blood pressure.
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DOI：
10.1097/hjh.0000000000000852
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发表时间：
2016-04
影响因子：
4.9
通讯作者：
Phillips SA
中科院分区：
文献类型：
--
作者：
Cavka A;Jukic I;Ali M;Goslawski M;Bian JT;Wang E;Drenjancevic I;Phillips SA
The aims of this study were to 1) test the hypothesis that short-term high salt (HS) intake reduces macro and micro vascular endothelial function in the absence of changes in blood pressure and 2) to determine if acute exercise restores endothelial function after HS in women. 12 women were administered high salt (HS; 11 g of sodium chloride for 7 days) and then underwent a weightlifting (WL) session. Brachial artery flow-mediated dilation (FMD) and nitroglycerin dilations (NTG) were measured with ultrasound at baseline, after HS, and after WL. Subcutaneous fat tissue biopsies were obtained at baseline and after HS and after WL. Resistance arteries (RA) from biopsies were cannulated for vascular reactivity measurements in response to flow (FID) and acetylcholine (ACh). Blood pressure was similar before and after HS diet. Brachial FMD was reduced after HS diet but was not affected by acute WL. Brachial NTG dilations were similar before and after HS. FID and ACh induced dilation (AChID) of RA were similar pre and post HS diet. FID and AChID was not altered by WL after HS diet. However, L-NAME significantly reduced FID at baseline and after exercise but had no effect dilator reactivity after HS diet alone. These data suggest that 1) HS intake reduces brachial artery endothelial function and switches the mediator of vasodilation in the microcirculation to a non-nitric oxide dependent mechanism in healthy adults and 2) acute exercise may switch the dilator mechanism back to NO during HS diet.
