Figure 4.
Vascular inflammation in hypertension: Outstanding questions and future directions. Dysregulated arachidonic acid metabolism in hypertension could impair the resolution of inflammation process via decreased production of endothelium-derived pro-resolving factors (e.g., lipoxins, resolvins, and protectins). Hypertension could stimulate the activity of vascular residing immune cells, such as macrophages or T cells, which could modulate vascular dysfunction by direct electrical coupling with vascular cells and/or production of pro-inflammatory cytokines directly into the vascular wall. Finally, newly identified components of hypertension-associated end organ injury, fibrocytes, could significantly contribute to vascular fibrosis and stiffening.
Abbreviations: AA, arachidonic acid; cGMP, cyclic guanosine monophosphate; COX, cyclooxygenase; eNOS, endothelial nitric oxide synthase; GTP, Guanosine-5’-triphosphate; L-arg, L-arginine; NO, nitric oxide; sGC, soluble guanylyl cyclase; TxA2; thromboxane A2