Please use this identifier to cite or link to this item: https://hdl.handle.net/2440/92049
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dc.contributor.advisorClifton, Peter Marshallen
dc.contributor.advisorKeogh, Jennifer Beatriceen
dc.contributor.authorDickinson, Kacie Marieen
dc.date.issued2014en
dc.identifier.urihttp://hdl.handle.net/2440/92049-
dc.description.abstractBackground: Increased dietary salt (sodium chloride) intake may increase the risk of cardiovascular disease independently of the effects on blood pressure by altering vascular endothelial function. It has previously been shown that reducing dietary salt intake can improve endothelial function after a short period of time however the effects of chronic moderate salt reduction and acute effects of a high salt meal on vascular function are not well studied in controlled trials. The thesis presents studies exploring the effects of manipulating dietary salt intake on endothelial function in normotensive overweight and obese and healthy adults. Aims: To assess the effects of 1) longer term moderate salt reduction on vascular function in overweight and obese adults 2) a high salt meal on post-prandial vascular function in healthy adults and 3) explore potential mechanisms underlying effects of acute and chronic modification of salt intake on vascular function. Results: In the first study overweight and obese adults (n=25) with normal blood pressure followed a moderately reduced salt diet (100mmol Na/day) and a usual salt diet (150mmol Na/day) for six weeks each in a randomised cross-over design. Following the reduced salt diet flow-mediated dilatation (FMD) was improved and endothelin-1 (a biomarker of endothelial function) improved significantly compared with the usual salt diet. The change in FMD occurred after two days, was sustained at 6 weeks and was significantly related to the change in 24hr urinary sodium to creatinine ratio. There were no changes in other markers of vascular stiffness (pulse wave velocity, augmentation index), plasma nitrate/nitrite, asymmetric dimethylarginine, renin, aldosterone or blood pressure between treatments. Population salt intakes are in excess of recommendations and published data suggest it may be common to consume in excess of 6g salt in a single meal. In the second study we tested the hypothesis that a high salt meal has adverse effects of vascular function in the postprandial period. The results showed that compared with a low salt meal (5mmol Na), the high salt meal (65mmol Na) impaired postprandial FMD and that the FMD response was not related to changes in blood pressure. In the third study, the mechanisms underlying the effects on endothelial function observed following the high salt meal in Study 2 were investigated. The results showed that augmentation index (a measure of arterial stiffness), serum sodium and osmolality increase significantly in response to the high salt meal (65mmol Na) compared with the low salt meal (5mmol Na). No differences in plasma nitrate/nitrite, vasopressin, atrial natriuretic peptide or blood pressure were observed between treatments. The main findings in of this thesis are that a modest reduction in dietary salt intake (3g/day) improves FMD rapidly after 2 days, which persists after 6 weeks, which may be explained by a fall in endothelin-1. Second, a single high salt meal has acute adverse effects on post-prandial arterial stiffness that is not accounted for by changes in plasma nitrate/nitrite or other vasoactive hormones. These results suggest mealtime sodium intakes as well as total daily salt intake may have implications for cardiovascular disease risk through altering endothelial function. Further work should be done to define the underlying short and long-term mechanisms by which salt affects endothelial function and long-term cardiovascular disease risk.en
dc.subjectsodium; salt; endothelial function; nitric oxide; blood pressureen
dc.titleEffects of dietary sodium intake on vascular function.en
dc.typeThesisen
dc.contributor.schoolSchool of Medical Sciencesen
dc.provenanceThis electronic version is made publicly available by the University of Adelaide in accordance with its open access policy for student theses. Copyright in this thesis remains with the author. This thesis may incorporate third party material which has been used by the author pursuant to Fair Dealing exceptions. If you are the owner of any included third party copyright material you wish to be removed from this electronic version, please complete the take down form located at: http://www.adelaide.edu.au/legalsen
dc.provenanceCopyright material removed from digital thesis. See print copy in University of Adelaide Library for full text.en
dc.description.dissertationThesis (Ph.D.) -- University of Adelaide, School of Medical Sciences, 2014en
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