Emerging evidence supports an important role for T cells in the genesis of hypertension. Because this work has predominantly been performed in experimental animals, we sought to determine whether human T cells are activated in hypertension. We employed a humanized mouse model in which the murine immune system is replaced by the human immune system. Angiotensin II increased systolic pressure to 162 mm Hg vs. 116 mm Hg for sham treated animals. Flow cytometry of thoracic lymph nodes, thoracic aorta and kidney revealed increased infiltration of human leukocytes (CD45+) and T lymphocytes (CD3+ and CD4+) in response to angiotensin II infusion. Interestingly, there was also an increase in the memory T cells (CD3+/CD45RO+) in the aortas and lymph nodes. Prevention of hypertension using hydralazine and hydrochlorothiazide prevented the accumulation of T cells in these tissues. Studies of isolated human T cells and monocytes indicated that angiotensin II had no direct effect on cytokine production by T cells or the ability of dendritic cells to drive T cell proliferation. We also observed an increase in circulating IL-17A producing CD4+ T cells and both CD4+ and CD8+ T cells that produce IFN-γ in hypertensive compared to normotensive humans. Thus, human T cells become activated and invade critical end-organ tissues in response to hypertension in a humanized mouse model. This response likely reflects the hypertensive milieu encountered in vivo and is not a direct effect of the hormone angiotensin II.

In hypertensive patients at high cardiovascular risk, OSA was associated with unfavourable prothrombotic fibrin clot characteristics, including hypofibrinolysis, which significantly improve as early as after 3 months of CPAP treatment.

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Background: Cardiovascular diseases are leading cause of death, disability and increased health care costs. Their development is determined by risk factors among which arterial hypertension (AH) is of crucial importance. Available data indicate significant role of inflammation in pathophysiology of AH. Lymphocyte T activation leads to endothelial dysfunction, increases procoagulability and atherosclerosis development. Aim of study was to evaluate activity of T lymphocytes in patients with AH and its modulation with antihypertensive treatment. Methods: Study group consisted of 56 subjects: 17 with 1st, 20 with 2nd stage AH and 19 healthy volunteers constituting control group. Antihypertensive therapy: in patients with 1st stage AH perindopril 5 mg once daily and in patients with 2nd stage AH bisoprolol (5 mg daily) additionally was ordered. At the beginning and after 4 weeks lymphocyte T activity determined by IL-2 and INF-γ release and hsCRP concentration was assessed using ELISA method. Results: hsCRP concentration was higher in hypertensive patients and difference was statistically significant in patients with stage 2 AH compared to control group (1.42 mg/L vs. 2.55 mg/L; p=0.003). Antihypertensive treatment was associated with hsCRP decrease but statistical significance was achieved only in the combination therapy arm. IL-2 concentration was increased in stage 1 AH by 14.8% (p=0.005) and in stage 2 AH group by 22.2% (p=0.002) compared to control group. Active treatment significantly reduced concentration of IL-2 in both groups. IFN-γ concentrations compared to the values obtained in the control group were higher: in stage 1 AH by 19.6% (p<0.001) and in stage 2 AH by 39.9% (p<0.001) accordingly. Results are shown in the table below.