Ace-inhibition with quinapril modulates the nitric oxide pathway in normotensive rats
Ace-inhibition with quinapril modulates the nitric oxide pathway in normotensive rats
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DOI：
10.1006/jmcc.2000.1311
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发表时间：
2001-03-01
影响因子：
5
通讯作者：
Ferrari, R
中科院分区：
文献类型：
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作者：
Bachetti, T;Comini, L;Ferrari, R
血管紧张素转换酶（ACE）抑制剂通过改善内皮功能发挥一些心血管益处。我们评估了在基线和炎症条件下，喹那普利（Q）长期治疗对正常血压大鼠（L）-精氨酸/一氧化氮（NO）通路的影响。缓激肽的作用也进行了研究。动物接受ACE抑制剂Q（1和10 mg/kg/天）给药1周。B-2、受体拮抗剂HOE 140、Q + HOE 140或无药物。在慢性治疗结束时，大鼠接受6小时的安慰剂或E。大肠杆菌内毒素挑战。进行以下测量：（i）内皮和诱导型NO合酶（eNOS和iNOS）蛋白表达;（ii）eNOS/iNOS活性;（iii）血清亚硝酸盐/硝酸盐和肿瘤坏死因子（TNF）-α水平;（iv）呼气中的NO（eNO）。Q增加基线主动脉eNOS蛋白表达（高达99%，P
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 B-2, 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)-alpha; (iv) NO in the expired air (eNO). Q increased baseline aortic eNOS protein expression (up to 99%, P