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.