Disruption of the kinin B1 receptor gene affects potentiating effect of captopril on BK-induced contraction in mice stomach fundus

被引:13
作者
Barbosa, Ana M. R. B. [1 ]
Felipe, Sandra A. [1 ]
Pesquero, Joao B. [1 ]
Paiva, Antonio C. M. [1 ]
Shimuta, Suma I. [1 ]
机构
[1] Univ Fed Sao Paulo, Escola Paulista Med, Dept Biophys, BR-04023062 Sao Paulo, Brazil
基金
巴西圣保罗研究基金会;
关键词
kinin B-1 receptor knockout; bradykinin; angiotensin converting enzyme; inhibitor;
D O I
10.1016/j.peptides.2006.09.010
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
A transgenic mouse model, deficient in kinin B-1 receptor (B-1(-/-)) was used to evaluate the role of B-2 receptor in the smooth muscle stomach fundus. The results showed that the potency of bradykinin (BK) to induce contraction in the gastric tissue was maintained whereas the efficacy was markedly reduced. The angiotensin converting enzyme (ACE) inhibitor captopril potentiated BK-induced effect in wild type (WT) but not in B-1(-/-) fundus. However, ACE activity detected by the convertion of Ang I to Ang II was inhibited by captopril in both types of gastric tissues. Taking into account the hypothesis that captopril and ACE bind to the B2 receptor, we suggest that this complex was not formed in the stomach deficient in B-1 receptor. Therefore, our finding strongly support the hypothesis that in smooth muscles that constitutively express the kinin B1 and B2 receptors, an interaction between captopril and ACE, B1 and B2 receptors should occur forming a complex protein interaction for the potentiating effect of ACE on kinin receptors. (c) 2006 Elsevier Inc. All rights reserved.
引用
收藏
页码:3377 / 3382
页数:6
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