engleski

Hypertension and immunity - what comes first?

Essential hypertension is a predominant pathological condition that is regarded as one of the most significant cardiovascular risk factors, and is a leading cause of morbidity and mortality worldwide. In medical textbooks hypertension is usually described as a disease characterized by endothelial dysfunction, altered sympathetic outflow and renal impairment. The role of immunity in hypertension is not mentioned even though there is considerable evidence that immunity may contribute to the development of hypertension. Experimental animals such as mice and rats which are lacking T cells are partially protected against both angiotensin II and salt-sensitive hypertension. However, the adoptive transfer of T cells restores blood pressure in these animals. Inflammatory cells accumulate in the kidneys and vasculature of humans and experimental animals with hypertension and are likely to contribute to end-organ damage. The central nervous system seems crucial in immune cell activation, because lesions in the anteroventral third ventricle block hypertension and T cell activation in response to angiotesni II. Likewise, genetic manipulation of reactive oxygen species in the subfornical organ modulates both hypertension and immune cell activation. Endothelial dysfunction may be caused by activation of innate immunity. Moreover, recent data show that cytokines released by inflammatory cells, including IL17, TNF-α, and IL6 lead to vascular dysfunction and remodeling. In addition, cytokines promote renal sodium retention, which leads to hypertension. Recent data from literature suggest that hypertension induces protein modification (innate immunity activation and reactive oxidative species production), then those proteins may become altered self antigens which includes T cell activation. Hypertensive humans also exhibit increased plasma levels of damage-associated molecular patterns which are strong activators of innate immunity through Toll like receptors. Moreover, activation of the immune system is induced by sympathetic outflow activation, and recent data confirm a link between the central nervous system and immunity. This data also indicate that the immune system is a permissive or causative factor in the development of hypertension.

Hypertension; immunity; TLR4

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