A novel role for the immune system in high blood pressure

Inflammation is implicated in the development of hypertension.

We found that endothelin-1 causes hypertension in mice and humans by modifying macrophage number and their phenotype.  Mouse macrophages and human monocytes express both ETA and ETB receptors, and show chemokinesis to endothelin-1. These immune cells then remove endothelin through ETB receptor-mediated endocytosis. Macrophage depletion amplifies the acute and chronic hypertensive response to ET-1. Mice with myeloid cell-specific ETB receptor deletion displayed an exaggerated hypertensive response to ET-1 and angiotensin II. In patients who received Mφ-depleting immunotherapy, blood pressure was higher and endothelial function worse than in those receiving non-depleting therapies. Overall, macrophages appear to play an important role in blood pressure control and potentially have a critical role as a therapeutic target in hypertension.

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