Introduction: Arterial hypertension (HTN) is a ma-jor cardiovascular disease (CVDs) risk factor, causing up to 7.5 million deaths worldwide. Despite multiple (non)pharmacological measures to prevent it/slow it down, HTN prompts 38% of heart diseases and 62% of strokes in developing countries.
Methods: Complex immune responses participate in the inflammatory process of HTN, variable endothelial aggressions trigger complex immune reactions whi-ch leads to a pro-inflammatory state. Reactive oxygen species (ROS) with a downstream product of cellular and soluble immune factors promotes endothelial dys-function and atherosclerosis. HTN can be mediated by the pleiotropic cytokine interleukin-6 (IL-6), through different signaling pathways such as signal transducer and activator of transcription -1, -3, and -5 (STAT) or Janus-associated kinase (JAK).
Results: Studies suggested that increased plasma levels of IL-6 and TNF-α, are independent risk factors for the development of high blood pressure in apparently healthy patients. More than, the relationship between this interleukin, angiotensin II and aldosterone could explain the role of IL-6 in HTN and provide a new the-rapeutic target.
Conclusions: Further studies are required in order to fully understand the implications of IL-6 in the patho-genesis of HTN and its end-organ damage and the pos-sible development of new antihypertensive drugs targe-ting inflammatory cytokines.