95 © Springer Nature Switzerland AG 2020 E. Agabiti-Rosei et al. (eds.), Microcirculation in Cardiovascular Diseases, Updates in Hypertension and Cardiovascular Protection, https://doi.org/10.1007/978-3-030-47801-8_8 Microvascular Endothelial Dysfunction in Hypertension Agostino Virdis and Stefano Masi 8.1 Introduction Endothelium represents the fundamental homeostatic tissue for the regulation of the vascular tone and structure, which is physiologically characterized by a balance between substances with vasodilating and antithrombogenic properties and sub- stances with vasoconstricting and prothrombotic activities. In healthy conditions, NO modulates several pathways leading to protect the vascular wall against those mechanisms involved in favouring and promoting the atherosclerotic disease. Under disease conditions, including essential hypertension, the endothelium loses its pro- tective role, becoming a pro-atherosclerotic structure [1]. The loss of the normal endothelial function is referred to as “endothelial dysfunction”, characterized by impaired NO bioavailability. This can be determined by either a reduced production of NO by endothelial NO synthase (eNOS) or, more frequently, an increased break- down by reactive oxygen species (ROS). Under such conditions, in addition to ROS, endothelial cells produce additional substances with vasoconstricting and prothrom- botic activities, including endothelin-1 (ET-1) and prostanoids [2, 3] generically called endothelial-derived contracting factors (EDCFs). The aim of this review is to give a brief overview of the known mechanisms involved in the pathogenesis of endothelial dysfunction in the microcirculation of hypertensive patients. A. Virdis (*) · S. Masi Department of Clinical and Experimental Medicine, University of Pisa, Pisa, Italy e-mail: agostino.virdis@med.unipi.it 8