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To 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. |
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