Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/12026
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dc.contributor.authorDickinson, Kacie Men
dc.contributor.authorClifton, Peter Men
dc.contributor.authorBurrell, Louise Men
dc.contributor.authorBarrett, P Hugh Ren
dc.contributor.authorKeogh, Jennifer Ben
dc.date.accessioned2015-05-16T01:39:44Z
dc.date.available2015-05-16T01:39:44Z
dc.date.issued2013-11-20en
dc.identifier.citationAtherosclerosis 2013; 232(1): 211-6en
dc.identifier.govdoc24401240en
dc.identifier.otherPUBMEDen
dc.identifier.urihttps://ahro.austin.org.au/austinjspui/handle/1/12026en
dc.description.abstractThe 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.en
dc.language.isoenen
dc.subject.otherArterial stiffnessen
dc.subject.otherNitric oxideen
dc.subject.otherSodiumen
dc.subject.otherAdolescenten
dc.subject.otherAdulten
dc.subject.otherAgeden
dc.subject.otherAtrial Natriuretic Factor.blooden
dc.subject.otherBlood Pressureen
dc.subject.otherC-Reactive Protein.metabolismen
dc.subject.otherChlorides.blooden
dc.subject.otherCross-Over Studiesen
dc.subject.otherEatingen
dc.subject.otherElectrolytes.blooden
dc.subject.otherEndothelium, Vascular.metabolismen
dc.subject.otherFemaleen
dc.subject.otherHealthy Volunteersen
dc.subject.otherHumansen
dc.subject.otherMaleen
dc.subject.otherMiddle Ageden
dc.subject.otherNitrates.blooden
dc.subject.otherNitric Oxide.blood.chemistryen
dc.subject.otherNitrites.blooden
dc.subject.otherOsmolar Concentrationen
dc.subject.otherPostprandial Perioden
dc.subject.otherSodium.blooden
dc.subject.otherSodium Chloride, Dietary.pharmacologyen
dc.subject.otherTime Factorsen
dc.subject.otherVascular Stiffness.drug effectsen
dc.subject.otherVasopressins.blooden
dc.subject.otherYoung Adulten
dc.titlePostprandial effects of a high salt meal on serum sodium, arterial stiffness, markers of nitric oxide production and markers of endothelial function.en
dc.typeJournal Articleen
dc.identifier.journaltitleAtherosclerosisen
dc.identifier.affiliationCommonwealth Scientific and Industrial Research Organisation, Animal, Food and Health Science, Adelaide, South Australia, Australiaen
dc.identifier.affiliationSchool of Pharmacy and Medical Sciences, Division of Health Sciences, University of South Australia, Adelaide, South Australia 5000, Australiaen
dc.identifier.affiliationThe National Health and Medical Research Council of Australia Centre of Clinical Research Excellence in Nutritional Physiology, Interventions and Outcomes, Adelaide, South Australia, Australiaen
dc.identifier.affiliationDiscipline of Physiology, Faculty of Health Science, University of Adelaide, South Australia, Australiaen
dc.identifier.affiliationDepartments of Medicine and Cardiology, Austin Health, University of Melbourne, Victoria, Australiaen
dc.identifier.affiliationMetabolic Research Centre, School of Medicine & Pharmacology & Faculty of Engineering, Computing and Mathematics, University of Western Australia, Perth, Western Australia, Australiaen
dc.identifier.doi10.1016/j.atherosclerosis.2013.10.032en
dc.description.pages211-6en
dc.relation.urlhttps://pubmed.ncbi.nlm.nih.gov/24401240en
dc.type.austinJournal Articleen
local.name.researcherBurrell, Louise M
item.openairetypeJournal Article-
item.cerifentitytypePublications-
item.grantfulltextnone-
item.fulltextNo Fulltext-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.languageiso639-1en-
crisitem.author.deptCardiology-
crisitem.author.deptGeneral Medicine-
crisitem.author.deptMedicine (University of Melbourne)-
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