Immunity and Hypertension

Hypertension is the primary cause of cardiovascular mortality. Despite multiple existing treatments, only half of those with the disease achieve adequate control. Therefore, understanding the mechanisms causing hypertension is essential for the development of novel therapies. Many studies demonstrate that immune cell infiltration of the vessel wall, kidney and central nervous system, as well as their counterparts of oxidative stress, the renal renin-angiotensin system (RAS) and sympathetic tone play a critical role in the development of hypertension. Genetically modified mice lacking components of innate and/or adaptive immunity confirm the importance of chronic inflammation in hypertension and its complications. Depletion of immune cells improves endothelial function, decreases oxidative stress, reduces vascular tone and prevents renal interstitial infiltrates, sodium retention and kidney damage. Moreover, the ablation of microglia or central nervous system perivascular macrophages reduces RAS-induced inflammation and prevents sympathetic nervous system activation and hypertension. Therefore, understanding immune cell functioning and their interactions with tissues that regulate hypertensive responses may be the future of novel antihypertensive therapies.

Automated summary

Studies have shown that immune cell infiltration and chronic inflammation play a critical role in the development of hypertension and its complications. Depletion of immune cells can improve endothelial function, reduce oxidative stress, lower vascular tone, and prevent kidney damage, indicating potential novel antihypertensive therapies through understanding immune cell functioning.