A New Role of Mister (MR) T in Hypertension
Mineralocorticoid Receptor, Immune System, and Hypertension
This article requires a subscription to view the full text. If you have a subscription you may use the login form below to view the article. Access to this article can also be purchased.
Emerging evidence has shown that inflammation and immunity play a central role in the genesis of hypertension. Cells of the immune system, including macrophages and T cells, have been observed in tissues of humans with hypertension and experimental evidence dating to the 1960s has suggested that both the elevation in blood pressure and end-organ damage are in part mediated by this immune cell infiltration. Studies in the past decade have shown that mice lacking T cells are protected against both angiotensin II and salt-sensitive hypertension and that adoptive transfer of T cells restores blood pressure in these animals. The T cells that accumulate in kidneys and vessels release inflammatory cytokines, including interleukin 17A, tumor necrosis factor-α, and interferon-γ (IFN-γ), that promote vascular dysfunction and renal damage.1 Macrophages and dendritic cells in tissues also release cytokines and metalloproteinases. These powerful signals affect vascular function by promoting vasoconstriction, remodeling, and fibrosis, and in the kidney, locally released cytokines alter renal tubular sodium reabsorption and antagonize pressure natriuresis.
Article, see p 1584
There is interest in the subsets of immune cells contributing to hypertension, with evidence supporting roles of CD8+ T cells, TH17 CD4+ T cells, B cells, monocytes, and monocyte-derived dendritic cells. Studies in mice and humans have emphasized a role of CD8+ T cells in hypertension, as these cells seem to be major sources of IFN-γ and an oligoclonal population of these cells accumulates in the kidney of hypertensive mice. Moreover, CD8−/− mice are partially protected against angiotensin II– and DOCA-salt–induced hypertension, whereas CD4−/− mice are not.2 There is an increased number of circulating senescent CD8+ T cells in humans with hypertension that produce IFN-γ, tumor necrosis factor-α, granzyme B and perforin and this is accompanied by a striking increase …