Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/22219
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dc.contributor.authorBaqar, Sara-
dc.contributor.authorKong, Yee Wen-
dc.contributor.authorChen, Angela X-
dc.contributor.authorO'Callaghan, Christopher J-
dc.contributor.authorMacisaac, Richard J-
dc.contributor.authorBouterakos, Maree-
dc.contributor.authorLambert, Gavin W-
dc.contributor.authorJerums, George-
dc.contributor.authorLambert, Elisabeth E-
dc.contributor.authorEkinci, Elif I-
dc.date2019-11-25-
dc.date.accessioned2019-12-04T05:00:32Z-
dc.date.available2019-12-04T05:00:32Z-
dc.date.issued2020-04-01-
dc.identifier.citationThe Journal of Clinical Endocrinology and Metabolism 2020; 105(4): dgz219en_US
dc.identifier.urihttps://ahro.austin.org.au/austinjspui/handle/1/22219-
dc.description.abstractTo determine if sympathetic nervous system (SNS) activation and endothelial dysfunction contribute to these observations, we examined the effect of salt supplementation on these systems in people with T2D with habitual low sodium. We hypothesized that salt supplementation will lower SNS activity and improve endothelial function compared to placebo. Randomized, double blinded, placebo-controlled, cross-over trial. Tertiary referral diabetes outpatients clinic. Salt supplementation (100mmol NaCl/24h) or placebo for three weeks was administered. Compared to placebo, salt supplementation increased MSNA (burst frequency p= 0.047, burst incidence p=0.016) however RHI (p=0.24), AI (p=0.201), ABPM (systolic p=0.09, diastolic p=0.14) and HRV were unaffected. Salt supplementation improved baroreflex (slope p=0.026), lowered aldosterone (p=0.004) and in salt-resistant individuals there was a trend towards improved RHI (p=0.07). In people with T2D and low habitual sodium intake, salt supplementation increased SNS activity without altering endothelial function or blood pressure but improved baroreflex function, a predictor of cardiac mortality. Salt-resistant individuals trended towards improved endothelial function with salt supplementation.en_US
dc.language.isoeng-
dc.subjectendothelial dysfunctionen_US
dc.subjectrenin-angiotensin-aldosterone systemen_US
dc.subjectsalt sensitivityen_US
dc.subjectsympathetic nervous systemen_US
dc.subjecttwenty-four-hour urinary sodium excretionen_US
dc.subjecttype two diabetesen_US
dc.titleEffect of salt supplementation on sympathetic activity and endothelial function in salt sensitive type 2 diabetes.en_US
dc.typeJournal Articleen_US
dc.identifier.journaltitleThe Journal of Clinical Endocrinology and Metabolismen_US
dc.identifier.affiliationEndocrinologyen_US
dc.identifier.affiliationGeneral Medicineen_US
dc.identifier.affiliationDepartment of Endocrinology & Diabetes, St Vincent's Hospital, Melbourne, Australiaen_US
dc.identifier.affiliationDepartment of Medicine, The University of Melbourne, Victoria, Australiaen_US
dc.identifier.affiliationClinical Pharmacology and Therapeuticsen_US
dc.identifier.affiliationHuman Neurotransmitters Laboratory, Baker IDI Heart & Diabetes Institute, Melbourne, Victoria, Australiaen_US
dc.identifier.affiliationIverson Health Innovation Research Institute and Faculty of Health, Arts and Design, Swinburne University of Technology, Victoria, Australiaen_US
dc.identifier.doi10.1210/clinem/dgz219en_US
dc.type.contentTexten_US
dc.identifier.orcid0000-0002-4921-1349en_US
dc.identifier.orcid0000-0003-2372-395Xen_US
dc.identifier.pubmedid31761946-
dc.type.austinJournal Article-
local.name.researcherEkinci, Elif I
item.grantfulltextnone-
item.openairetypeJournal Article-
item.languageiso639-1en-
item.fulltextNo Fulltext-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.cerifentitytypePublications-
crisitem.author.deptClinical Pharmacology and Therapeutics-
crisitem.author.deptEndocrinology-
crisitem.author.deptEndocrinology-
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