Article Text
Abstract
Objective: Low sodium intake may trigger sympathetic nervous system (SNS) activation and endothelial dysfunction. Studies have not explored these associations along the glucose continuum. Accordingly, we compared endothelial function and SNS activity in individuals with low sodium intake and differing categories of metabolic risk along the glucose continuum. We hypothesized that low sodium intake is associated with (1) impairment of endothelial function and (2) higher SNS activity in individuals with higher metabolic risk. Research Design and Methods: In this prospective observational study, participants (n=54) with low sodium intake (single 24 hours urine sodium excretion <150 mmol/24 hours) were categorized based on oral glucose tolerance testing as: normal glucose tolerance (NGT, n=10), impaired glucose tolerance (IGT, n=15), treatment naive type 2 diabetes (T2D−) (n=12) or treated type 2 diabetes (T2D+) (n=17). We assessed endothelial function using pulse amplitude tonometry (PAT) derived reactive hyperemic index and PAT ratio; arterial stiffness via augmentation index; muscle sympathetic nerve activity (MSNA) using microneurography; cardiac baroreflex; heart rate; blood pressure; glycosylated hemoglobin A1c (HbA1c) and lipid profile. Results: Mean (SD) sodium excretion was 110.6 (26) mmol/24 hours. Compared with NGT, IGT and T2D−, the T2D+ group had lower MSNA (p=0.005), PAT ratio (p=0.04) and baroreflex sensitivity (p=0.0002) and an augmented heart rate (p=0.02). The T2D+ group had appropriate mean (SD) glycemic (HbA1c 7.2 (1.72)%), total cholesterol (4.2 (1.0) mmol/L), low-density lipoprotein (2.2 (1.0) mmol/L) and blood pressure (systolic 136 (13), diastolic 78 (12)) (mm Hg) control. Conclusions: Individuals with T2D+ have impaired endothelial and baroreflex function, despite low sodium intake, appropriately managed cardiometabolic risk factors and lower SNS activity, compared with others along the glucose continuum. Whether low sodium intake is associated with modulation of the sympathovascular profile in T2D requires further investigation.
- cardiovascular disease
- endothelial dysfunction
- impaired glucose tolerance
- microneurography
- pulse amplitude tonometry
- sympathetic nervous system
- twenty four hour urinary sodium excretion
- type 2 diabetes
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Footnotes
Contributors SB, EIE and EL conceived the study and selected participants from the Department of Endocrinology, Austin Health and the Human Neurotransmitter Laboratory, Baker IDI databases respectively and interpreted the data. SB, NS and YWK collected clinical data. EL performed microneurographic recordings and analyses. SB performed the statistical analyses, wrote and revised the manuscript. All authors critically read and approved the final content of the manuscript. SB is the guarantor of this work and, as such, had full access to all the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis.
Funding EIE was supported by an NHMRC Early Career Research Fellowship (#1054312), Viertel Clinical Investigatorship, Sir Edward Weary Dunlop Medical Research Foundation grant, Royal Australian College of Physicians fellowship and Diabetes Australia Research Program Grant. SB was supported by a National Heart Foundation Health Professional Scholarship (100287).
Competing interests None declared.
Patient consent for publication Not required.
Ethics approval The study protocol was approved by the Human Research Ethics Committee at the Austin Health as well the Baker Heart and Diabetes Institute and Alfred Health.
Provenance and peer review Not commissioned; externally peer reviewed.
Data sharing statement There is no additional data from this study.