FIG. 7.

Role of HO-1/CO in hypertension. As Ang II in blood stream causes hypertension, chronic exposure of Ang II in spontaneously hypertensive rats induces hypertension. CO, like NO, activates sGC and cGMP pathway and can open potassium channels in VSMCs. This reduces vascular contractility and BP. Hypertension increases soluble VEGFs, soluble endoglins, and tumor necrosis factor-α, accompanied by low level of HO-1 activity. Upregulating HO-1 expression in myofibroblasts and infiltrated inflammatory cells reduces BP. Upregulation of aortic HO-1 protects tissue damage from high BP by reducing inflammatory response. HO-1 inducers or HO-1 gene/CO delivery may efficiently protect tissue damages by vascular inflammation and vascular remodeling. Ang II, angiotensin II; BP, blood pressure; sGC, soluble guanylyl cyclase; VEGF, vascular endothelial growth factor; VSMC, vascular SMC.