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首页> 外文期刊>Japanese Journal of Pharmacology >Difference among Angiotensin-Converting Enzyme Inhibitors in Potentiating Effects on Bradykinin-Induced Microvascular Leakage in Guinea Pig Airways
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Difference among Angiotensin-Converting Enzyme Inhibitors in Potentiating Effects on Bradykinin-Induced Microvascular Leakage in Guinea Pig Airways

机译：血管紧张素转换酶抑制剂对缓激肽诱导的豚鼠气道微血管渗漏增强作用的差异

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References(39) Cited-By(5) We investigated the effect of imidapril, a novel angiotensin-converting enzyme (ACE) inhibitor, on augmentation of airway microvascular leakage induced by bradykinin (BK) and substance P (SP) in guinea pigs and compared it with those of enalapril and captopril. The three ACE inhibitors significantly potentiated BK- and SP-induced airway microvascular leakage in a dose-dependent manner. In spite of the compatible or higher ACE inhibitory activity of imidapril, its potentiating activity in BK-induced leakage was lower than those of enalapril and captopril both by single administration (0.3-30 mg/kg, p.o.) and repeated administration for eight days (0.1-10 mg/kg/day, p.o.). The potentiating activities of the three ACE inhibitors were suppressed by pretreatment with a BK2-receptor antagonist, but not by neurokinin 1 and neurokinin 2 antagonists, suggesting that neurokinins may not be involved in BK-induced leakage under the conditions used. On the other hand, the potentiating effect of imidapril in SP-induced leakage was weaker than those of enalapril and captopril only after single high doses. The present study shows that the ACE inhibitors have different activity in potentiation of the airway microvascular leakage induced by BK, which may be ascribable to the difference in their inhibition of BK hydrolysis. This evidence may partly explain the smaller incidence of dry cough induced by imidapril compared with other ACE inhibitors when clinically used as antihypertensive drugs.
机译：参考文献（39）Cited-By（5）我们研究了一种新型血管紧张素转换酶（ACE）抑制剂咪达普利对豚鼠和豚鼠体内缓激肽（BK）和P物质（SP）诱导的气道微血管渗漏增强的作用。与依那普利和卡托普利比较。三种ACE抑制剂以剂量依赖性方式显着增强BK和SP诱导的气道微血管渗漏。尽管咪达普利具有相称或更高的ACE抑制活性，但通过单次给药（0.3-30 mg / kg，口服）和重复给药8天（BK）诱导的渗漏，其增强活性均低于依那普利和卡托普利。 0.1-10 mg / kg /天，口服）。三种ACE抑制剂的增强活性被BK2受体拮抗剂预处理抑制，但神经激肽1和神经激肽2拮抗剂未抑制，这表明在所用条件下神经激肽可能不参与BK诱导的渗漏。另一方面，仅在单次高剂量后，咪达普利在SP诱导的渗漏中的增强作用就弱于依那普利和卡托普利。本研究表明，ACEI抑制剂在增强BK诱导的气道微血管渗漏方面具有不同的活性，这可能归因于其对BK水解的抑制作用的差异。当临床上将其用作降压药时，这一证据可能部分解释了与其他ACE抑制剂相比，吡虫啉引起的干咳的发生率更低。

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