Introduction
Hypertension remains a leading cause of global death and disability from cardiovascular disease and stroke. High blood pressure afflicts more than 1 billion people worldwide. The borders between normotension and hypertension are arbitrary. In the recent update of the ”Guideline for the Prevention, Detection, Evaluation, and Management of High Blood Pressure in Adults” the border for stage 1 hypertension was lowered by 10 mmHg and starts now at 130 mmHg (Whelton et al., 2017). In consequence, the number of hypertensive patients increased i.e. in the United States over night from 32% to 43% of the American population (Wenzel et al., 2019).
In spite of this high prevalence of the disease and decades of research on the subject, the etiology of most cases of hypertension remains undefined (Montaniel & Harrison, 2016). An important development in the field of hypertension has been the realization that there is an immunologic contribution to the disease (Guzik et al., 2007; Norlander et al., 2018; Wenzel et al., 2016). The complement system has long been viewed as a complex network mainly serving innate immune functions. A growing body of evidence has accumulated demonstrating, that the functions of complement go beyond innate immunity. New discoveries in inflammatory diseases refine our appreciation of the close interdependency of “ancient” complement and “modern” adaptive immune mechanisms. Uncontrolled complement activation can cause autoimmunity, tissue inflammation and injury, and complement-inhibitory drugs are effective treatments for several inflammatory diseases. Arterial hypertension is a new field in complement research (Ward, 2016). Blood pressure elevation induces the activation of complement system and production of complement factors. These factors accelerate the progression of vascular injury and promote the development of hypertension via two different kinds of regulation. First, complement factors directly promote vascular cell dysfunction through their specific receptors in effector cells. In addition, complement activation mediates immune cell recruitment and induces inflammatory factor production in these cells. This includes cells of the innate and adaptive immune system. These together aggravate hypertension-induced organ damage (Ruan & Gao, 2019).
Here, we update the current knowledge about the role of complement in arterial hypertension (Chen et al., 2020a; Ruan & Gao, 2019; Wenzel et al., 2017) and extend a summary towards what its known in the processes underlying hypertensive end organ damage.