Ace-inhibition with quinapril modulates the nitric oxide pathway in normotensive rats

Angiotensin-converting enzyme (ACE) inhibitors exert some cardiovascular benefits by improving endothelial function. We evaluated the effects of chronic treatment with quinapril (Q) on the L-arginine/nitric oxide (NO) pathway in normotensive rats under baseline and inflammatory conditions. The role of bradykinin was also investigated. The animals received for 1 week either the ACE-inhibitor Q (1 and 10 mg/kg/day), the B₂ receptor antagonist HOE 140. Q + HOE 140, or no drug. At the end of chronic treatment, rats underwent either a 6-h placebo or an E. coli endotoxin challenge. The following measurements were made: (i) endothelial and inducible NO synthase (eNOS and iNOS) protein expression: (ii) eNOS/iNOS activity: (iii) serum levels of nitrite/nitrate and tumour necrosis factor (TNF)-α; (iv) NO in the expired air (eNO). Q increased baseline aortic eNOS protein expression (up to 99%, P