Figure 10.

Effect of zofenopril on H₂S and NO bioavailability. By inhibiting myocardial angiotensin converting enzyme (ACE) activity, zofenopril reduces the generation of angiotensin II and increases levels of bradykinin (BK). BK, through stimulation of endothelial B₂ receptors, promotes the release of NO, prostacyclin, and endothelium‐derived hyperpolarizing factor (EDHF), which in turn leads to cardioprotection. On the other hand, zofenopril, by releasing H₂S, enhances tissue antioxidant defense and promotes eNOS activation, leading to increased levels of NO. Therefore, ACE inhibition, H₂S, and NO account for zofenopril‐mediated cardioprotective effects.