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.

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