ACE inhibitors block the generation of angiotensin II and prevent the breakdown of bradykinin.
Bradykinin, a potent endothelium-dependent vasodilator, causes contraction of non-vascular smooth muscle, increases vascular permeability and also is involved in the mechanism of pain. It works on the blood vessels through the release of prostacyclin, nitric oxide, and Endothelium-Derived Hyperpolarizing Factor.
ACE inhibitors improve endothelial dysfunction in patients with coronary disease and have been shown to stimulate angiogenesis and collateral vessel formation in a rabbit ischemic hindlimb model.
