Endothelial Dysfunction in Experimental Models of Arterial Hypertension: Cause or Consequence?
Figure 1
A brief scheme of interactions among the individual endothelium-derived factors and their mechanisms of action in the endothelial cells. Abbreviations are explained in the list of abbreviations. The activation of the appropriate receptor by its agonist as well as shear stress leads to alterations in the intracellular calcium concentration in the endothelial cells which affect the activity of all NOS, CSE, NOX, and PLA2 resulting in the release of NO, H2S, ROS, and AA-derived metabolites, respectively. ROS can further inhibit (marked by “−” sign) the production of PGI2 and to elevate TXA2 and Ang-II production. In addition, there are significant interactions among the NO, H2S, and superoxide as well as among NO, Ang-II, ET-1, and HETEs. Individual EDRFs then affect the vascular smooth muscle cells, via modulation of the appropriate receptors or channels, resulting in the respective vascular smooth muscle cell relaxation and constriction.
