— Ulrich Wenzel, MD
Increasing evidence indicates that hypertension and hypertensive end-organ damage are not only mediated by hemodynamic injury. Inflammation plays also an important role in the pathophysiology and contributes to the deleterious consequences of arterial hypertension. Sodium intake is indispensable for normal body function but can be detrimental when taken in excess because of dietary requirements. Recent data show that sodium levels also modulate the function of monocyte/macrophages, dendritic cells, and different T cell subsets. Some of these effects are mediated by changes in the microbiome and metabolome that can be found after high salt intake.
The purpose of our work is to discover the mechanisms underlying arterial hypertension to better understand arterial hypertension and the resulting end-organ damage. We focus on three points:
Figure 1: Our current concept explaining arterial hypertension (from Hengel et al. 2022). We call it a modified mosaic theory putting inflammation and salt in the center.
Figure 2: Proinflamamtory effects of the mineralocorticoid receptor in innate and adaptive immune cells (from Hengel et al 2022). Recent data suggest that the mineralocorticoid receptor is expressed in inflammatory cells and has proinflammatory effects.
Figure 3: The pathogenesis of renal injury in so-called malignant nephrosclerosis is not understood. It is a form of thrombotic microangiopathy defined by progressive narrowing of interlobular arterial branches and afferent arterioles with intima fibrosis and onion-like appearance of intimal scarring as shown below (histology provided by T. Wiech).
©Ulrich Wenzel
Senior Physician
III. Department of Medicine, University Medical Center Hamburg-Eppendorf (UKE)
Martinistr. 52
20246 Hamburg, Germany
Senior Physician
1983 - 1989
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Medical School, Freie Universität Berlin, Germany |
2002 - 2020
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Habilitation and Venia legendi Internal Medicine, University Medical Center Hamburg Eppendorf, UKE |
1992
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Medical Thesis, Freie Universität Berlin |
Clinical postgraduate education:
2005
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Hypertensiologe DHL® |
2004
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Board Certification Nephrology |
2000
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Board Certification Internal Medicine |
Scientific postgraduate education:
1993 - 1995
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Post-Doc, University of Texas, Health Science Center at San Antonio, Department of Medicine, Division of Nephrology (H. Abboud, M. D., Professor of Medicine), San Antonio, Texas, USA |
2020 - 2023 - 2020
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President German Society of Hypertension |
2016
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Franz Gross Award, Germany Society of Hypertension |
2003
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Dr. Martini-Award, Hamburg, Germany |
2001
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Adalbert Buding Award, Germany Society of Hypertension |
1988 - 1989
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Fellow Studienstiftung des Deutschen Volkes |
1. | Bode M, Herrnstadt GR, Dreher L, Ehnert N, Kirkerup P, Lindenmeyer MT, Meyer-Schwesinger CF, Ehmke H, Köhl J, Huber TB, Krebs CF, Steinmetz OM, Wiech T, Wenzel UO. Hypertension. 2024 Jan;81(1):138-150. |
2. | Bode M, Diemer JN, Luu TV, Ehnert N, Teigeler T, Wiech T, Lindenmeyer MT, Herrnstadt GR, Bülow J, Huber TB, Tomas NM, Wenzel UO. Br J Pharmacol. 2023, 180:2412-2435. |
3. | The role of the mineralocorticoid receptor in immune cells in cardiovascular disease. |
4. | Mosaic theory revisited: inflammation and salt play a central role in arterial hypertension. |
5. | The role of complement in arterial hypertension and hypertensive end organ damage.. |
6. | The chemokine receptor CX3CR1 reduces renal injury in mice with angiotensin II-induced hypertension. |
7. | Adaptive immunity and IL-17A in chronic kidney disease in mice. |
8. | Salt, inflammation, IL-17 and hypertension. |
9. | The complement receptor C5aR1 contributes to renal damage but protects the heart in angiotensin II-induced hypertension. |
10. | Immune Mechanisms in Arterial Hypertension. |
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