Abstract: TH-OR055
Sodium-Sensitive Blood Pressure Response in Type 1 Diabetes Is Accompanied by Impeded Skin Lymphangiogenesis
Session Information
- Hypertension: Off the Cuff - Treatment and Mechanisms
November 02, 2017 | Location: Auditorium C, Morial Convention Center
Abstract Time: 05:18 PM - 05:30 PM
Category: Hypertension
- 1104 Hypertension: Clinical and Translational - Salt and Hypertension
Authors
- Wenstedt, Eliane F.E., Academic Medical Center, Amsterdam, Netherlands
- Rorije, Nienke M.G., Academic Medical Center, Amsterdam, Netherlands
- Olde Engberink, Rik Hg, Academic Medical Center, Amsterdam, Netherlands
- Van den born, Bert-jan, Academic Medical Center, Amsterdam, Netherlands
- Aten, Jan, Academic Medical Center, Amsterdam, Netherlands
- Vogt, Liffert, Academic Medical Center, Amsterdam, Netherlands
Background
Studies showed that sodium can be non-osmotically stored within the skin. In response to high sodium diet (HSD), skin sodium content increases and macrophages are attracted, inducing lymphangiogenesis. Disruption of this system has been shown to lead to sodium-sensitive hypertension. This study investigates the effects of HSD on skin lymphatic and blood capillaries as well as blood pressure (BP) in type 1 diabetic patients (DM1).
Methods
We performed a randomized crossover study in males with DM1 and healthy controls. All subjects pursued an 8-day low sodium diet (LSD: <50 mmol Na+/day) and HSD (>200 mmol Na+/day). Diet order was randomized and time in-between diets was 1-2 weeks. After each diet, BP measurements and skin biopsies were obtained. Macrophages (CD68), vascular endothelium (CD31) and lymphatic endothelium (D2-40) were identified through immunohistochemistry.
Results
This study included 8 patients with DM1 and 12 controls who were similar regarding age, BMI and eGFR. In DM1 patients, mean arterial pressure was higher after HSD as compared to LSD (mean (SE) 85(2) vs. 80(1) mmHg, p=0.03) whereas in controls no differences were observed (78(1) vs. 78(2) mmHg, p=0.66). HSD increased lymphatic cross sectional surface area in controls (p=0.01) but not in DM1 patients (fig 1a). Less CD68+ macrophages were present in DM1 patients compared to controls (p<0.001) (fig 1b). In both groups, there was a strong association between lymphatic capillary density and macrophage density (DM1 r=0.57 p=0.02; controls r=0.71 p=0.02).
Conclusion
The sodium-sensitive BP increase in DM1 patients is accompanied by impeded skin lymphangiogenesis and reduced skin macrophage content. Lymphangiogenesis may help to prevent sodium-sensitive hypertension.