Introduction Patients with type 1 diabetes are susceptible to hypertension, possibly resulting from increased salt sensitivity and accompanied changes in body fluid composition. We examined the effect of a high-salt diet (HSD) in type 1 diabetes on hemodynamics, including blood pressure (BP) and body fluid composition.
Research design and methods We studied eight male patients with type 1 diabetes and 12 matched healthy controls with normal BP, body mass index, and renal function. All subjects adhered to a low-salt diet and HSD for eight days in randomized order. On day 8 of each diet, extracellular fluid volume (ECFV) and plasma volume were calculated with the use of iohexol and 125I-albumin distribution. Hemodynamic measurements included BP, cardiac output (CO), and systemic vascular resistance.
Results After HSD, patients with type 1 diabetes showed a BP increase (mean arterial pressure: 85 (5) mm Hg vs 80 (3) mm Hg; p<0.05), while BP in controls did not rise (78 (5) mm Hg vs 78 (5) mm Hg). Plasma volume increased after HSD in patients with type 1 diabetes (p<0.05) and not in controls (p=0.23). There was no significant difference in ECFV between diets, while HSD significantly increased CO, heart rate (HR) and N-terminal pro-B-type natriuretic peptide (NT-proBNP) in type 1 diabetes but not in controls. There were no significant differences in systemic vascular resistance, although there was a trend towards an HSD-induced decrease in controls (p=0.09).
Conclusions In the present study, patients with type 1 diabetes show a salt-sensitive BP rise to HSD, which is accompanied by significant increases in plasma volume, CO, HR, and NT-proBNP. Underlying mechanisms for these responses need further research in order to unravel the increased susceptibility to hypertension and cardiovascular disease in diabetes.
Trial registration numbers NTR4095 and NTR4788.
- extracellular fluid volume
- plasma volume
- salt sensitivity
- systemic vascular resistance
- type 1 diabetes
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Contributors Conceptualization: LV and B-JHvdB; investigation: NMGR and RHGOE; analysis: EFEW, KMvdM, YC, and AHJD; writing of the original draft: EFEW; writing, review and editing: all coauthors; visualization: EFEW; supervision: LV and B-JHvdB; funding acquisition: LV. All authors read and approved the final manuscript.
Funding This work was supported by the Dutch Kidney Foundation (Kolff grant number KJPB 11.22 to LV) and The Netherlands Organization for Health Research and Development (clinical fellowship grant number 90700310 to LV).
Competing interests None declared.
Patient consent for publication Not required.
Ethics approval The studies were conducted in the Amsterdam UMC, location AMC, The Netherlands, after approval of the local ethics committee (METC AMC, 013_041 and 2014_074), and were in accordance with the Declaration of Helsinki. All participants gave written informed consent. The extensive nature of the study protocol led to the recommendation by our ethics committee to register the trial with separate protocols for each patient group.
Provenance and peer review Not commissioned; externally peer reviewed.
Data availability statement Data are available upon reasonable request. The datasets used and/or analyzed during the current study are available from the corresponding author on reasonable request.
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