Disruption of the kinin B1 receptor gene affects potentiating effect of captopril on BK-induced contraction in mice stomach fundus.
Peptides
; 27(12): 3377-82, 2006 Dec.
Article
em En
| MEDLINE
| ID: mdl-17079052
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 B(2) 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 B(1) and B(2) receptors, an interaction between captopril and ACE, B(1) and B(2) receptors should occur forming a complex protein interaction for the potentiating effect of ACE on kinin receptors.
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Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Inibidores da Enzima Conversora de Angiotensina
/
Captopril
/
Receptor B1 da Bradicinina
/
Mucosa Gástrica
/
Contração Muscular
Tipo de estudo:
Prognostic_studies
Limite:
Animals
Idioma:
En
Revista:
Peptides
Ano de publicação:
2006
Tipo de documento:
Article
País de afiliação:
Brasil
País de publicação:
Estados Unidos