Hypertension, Inflammation and the Renin Angiotensin System

Increasing evidence indicates that inflammation contributes to the deleterious consequences of arterial hypertension and its end-organ damage of this disease. Renal inflammation results in injury and impaired urinary sodium excretion. Modulation of the immune response can reduce the severity of blood pressure elevation and hypertensive end-organ damage in several animal models. The underlying mechanisms are incompletely understood. We wish to address the role of the innate and the adaptive immune system in hypertension and hypertensive end organ damage by examining the following points:

1. Role of IL-17 in arterial hypertension

2. Role of complement in arterial hypertension

3. Role of dendritic cells in arterial hypertension

In addition, we are working on new models of arterial hypertension with hypertensive cardiac and renal injury in mice. In addition, we are examining the role of the soluble (pro)renin receptor in hypertension and chronic kidney disease.

Working hypothesis describing the role of immunity in hypertension
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Working hypothesis describing the role of immunity in hypertension
Hypertensive factors like Ang II, salt or aldosterone lead to a cascade of events: They directly activate the innate immune system.
Mouse models of hypertension, kidney disease and inflammation
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Mouse Models of Hypertension, Kidney Disease & Inflammation
FACS analysis heart, aorta, kidney & Hemodynamic measurements
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FACS Analysis Heart, Aorta, Kidney & Hemodynamic Measurements

Team members

Ulrich Wenzel
Prof. Dr. med.
Ulrich Wenzel
  • Facharzt für Innere Medizin und Nephrologie

Dr. Alva Rosendahl a.rosendahl@uke.de

Stefan Gatzemeier, BTA

Daniel Czesla, Doktorand

Sebastian Weiss, Doktorand

Erfan Ahadzadeh , Doktorand

Prof. Dr. Heimo Ehmke cooperation partner from the Dept. of Physiology