Purpose of review: Several studies published in the past three decades have suggested that inflammation and activation of immunity are central features in the pathogenesis of atherosclerosis, ischemic myocardial injury, and also in hypertension-induced target organ damage. A better understanding of this field could help us to explain the increased cardiovascular risk in patients with chronic inflammation.
Recent findings: Recent studies have demonstrated that macrophages and various T-cell subtypes play a pivotal role in the regulation of blood pressure and target organ damage. Hypertensive stimuli such as the effector molecule of the renin-angiotensin system, angiotensin II, not only regulate vascular tone and sodium balance, but also activate immune cells and promote cell infiltration into target organs. Experimental and clinical evidence show that adaptive transfer of immune cells, rendering mice deficient for a certain subset of immune cells, or immunosuppressive treatment affects blood pressure and ameliorates target organ damage.
Summary: The aim of this review is to summarize and discuss some of the more recent insights as to how immune cells might affect the regulation of blood pressure and the pathogenesis of hypertension-induced target organ damage.