1. Nat. Rev. Nephrol. doi:10.1038/nrneph.2017.178
Figure 1 Novel mechanisms of hypertension and aortic aneurysm formation
Figure 1 | Novel mechanisms of hypertension and aortic aneurysm formation. Salt induces activation of T helper 17 (TH17) cells via a serum and glucocorticoid-regulated kinase 1 (SGK1)- dependent pathway that enhances the activity of Na+/K+/2Cl− cotransporter 1 (NKCC1). High salt intake also results in depletion of Lactobacillus spp. in the intestinal microbiome, leading to stimulation of TH17 cells. Angiotensin II (ANGII) stimulates γδT cells, which in turn prime other immune cells, including TH17 cells. Activated TH17 and γδT cells produce IL‑17, which stimulates renal sodium retention and vasoconstriction, resulting in increased blood pressure. Rare renin– angiotensin–aldosterone system (RAAS) gene variants increase the salt sensitivity of blood pressure, potentially via a mechanism involving ANGII. In perivascular visceral adipose tissue, binding of ANGII to type 1a angiotensin II receptor (AGTR1A) leads to increased production of pro-inflammatory osteopontin, which contributes to the formation and progression of abdominal aortic aneurysms.
Schiffrin, E. L. (2017) Novel mechanisms of hypertension and vascular dysfunction
Nat. Rev. Nephrol. doi: /nrneph