Temocapril

Pieper GM, et al. European Journal of Pharmacology, 2000, 403, 129-132.

In a well-controlled experimental model of diabetes mellitus, the angiotensin-converting enzyme (ACE) inhibitor temocapril was evaluated for its ability to prevent vascular endothelial dysfunction, a hallmark of diabetic vascular complications. Aortic ring segments were harvested from diabetic rats and mounted in an organ bath system to assess vascular responsiveness. Endothelium-dependent relaxation was induced by cumulative addition of acetylcholine (ACh), whereas endothelium-independent relaxation was assessed using nitroglycerin.
Diabetic aortic rings exhibited markedly impaired ACh-induced relaxation, while responses to nitroglycerin remained unaffected, indicating selective endothelial dysfunction. Chronic oral administration of temocapril effectively preserved endothelium-dependent relaxation responses. Notably, ACh-induced vasodilation in the temocapril-treated group remained largely mediated by nitric oxide (NO), as evidenced by partial attenuation upon NOS inhibition using l-nitroarginine. However, a residual NO-independent component suggested potential alternative vasodilatory pathways activated by temocapril treatment.
These findings demonstrate the experimental use of temocapril in organ bath-based vascular reactivity assays, underscoring its potential to restore endothelial function in diabetic models by preserving NO bioavailability and possibly enhancing endothelial resilience through additional mechanisms.