High blood pressure—or hypertension—is triggered by angiotensin II. This hormone instructs the kidneys to retain salt and the brain to release stress hormones. It also activates oxidases that generate free radicals, which narrow blood vessels and cause plaques to grow and harden the arteries.

Recent evidence suggests that angiotensin II might also get the immune system into the tension-raising act. Patients with immune systems weakened by immunosuppressive drugs or HIV infection have low blood pressure, which can skyrocket when they go off the drugs or start taking antiviral medications. One set of lymphocytes, the T cells, are the likeliest culprits, as they bear angiotensin II receptors and the same dangerous free radical–generating enzymes.

Guzik et al. now find that angiotensin II activates T cells to raise blood pressure. Mice that lack lymphocytes failed to develop hypertension after angiotensin II injection unless T cells were put back in. The hormone, they found, increased the T cells' ability to attach to and infiltrate blood vessel walls. The cells congregated in the underlying fatty tissue and secreted the inflammatory cytokine tumor necrosis factor (TNF), which further activates free radical production in the surrounding cells. Blocking TNF blunted hypertension.

The authors propose that T cells infiltrating the kidney and the brain might also amplify angiotensin II's damaging effects in these organs.

Related Article

Role of the T cell in the genesis of angiotensin II–induced hypertension and vascular dysfunction

Tomasz J. Guzik, Nyssa E. Hoch, Kathryn A. Brown, Louise A. McCann, Ayaz Rahman, Sergey Dikalov, Jorg Goronzy, Cornelia Weyand, and David G. Harrison
J. Exp. Med. 2007 204: 2449-2460. [Abstract] [Full Text] [PDF]