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首页> 外文期刊>Canadian Journal of Physiology and Pharmacology >Angiotensin-(1-7) potentiates responses to bradykinin but does not change responses to angiotensin I.
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Angiotensin-(1-7) potentiates responses to bradykinin but does not change responses to angiotensin I.

机译：血管紧张素-（1-7）可增强对缓激肽的反应，但不会改变对血管紧张素I的反应。

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摘要

Angiotensin-(1-7) (Ang-(1-7)), a bioactive peptide in the renin-angiotensin system, has counterregulatory actions to angiotensin II (Ang II). However, the mechanism by which Ang-(1-7) enhances vasodepressor responses to bradykinin (BK) is not well understood. In the present study, the effects of Ang-(1-7) on responses to BK, BK analogs, angiotensin I (Ang I), and Ang II were investigated in the anesthetized rat. The infusion of Ang-(1-7) (55 pmol/min i.v.) enhanced decreases in systemic arterial pressure in response to i.v. injections of BK and the BK analogs [Hyp3, Tyr(Me)8]-bradykinin (HT-BK) and [Phe8psi (CH2-NH) Arg9]-bradykinin (PA-BK) without altering pressor responses to Ang I or II, or depressor responses to acetylcholine and sodium nitroprusside. The angiotensin-converting enzyme (ACE) inhibitor enalaprilat enhanced responses to BK and the BK analog HT-BK without altering responses to PA-BK and inhibited responses to Ang I. The potentiating effects of Ang-(1-7) and enalaprilat on responses to BK were not attenuated by the Ang-(1-7) receptor antagonist A-779. Ang-(1-7)- and ACE inhibitor-potentiated responses to BK were attenuated by the BK B2 receptor antagonist Hoe 140. The cyclooxygenase inhibitor sodium meclofenamate had no significant effect on responses to BK or Ang-(1-7)-potentiated BK responses. These results suggest that Ang-(1-7) potentiates responses to BK by a selective B2 receptor mechanism that is independent of an effect on Ang-(1-7) receptors, ACE, or cyclooxygenase product formation. These data suggest that ACE inhibitor-potentiated responses to BK are not mediated by an A-779-sensitive mechanism and are consistent with the hypothesis that enalaprilat-induced BK potentiation is due to decreased BK inactivation.
机译：血管紧张素-（1-7）（Ang-（1-7））是肾素-血管紧张素系统中的一种生物活性肽，对血管紧张素II（Ang II）具有反调节作用。但是，Ang-（1-7）增强对缓激肽（BK）的血管舒缩剂反应的机制尚不清楚。在本研究中，在麻醉的大鼠中研究了Ang-（1-7）对BK，BK类似物，血管紧张素I（Ang I）和Ang II的反应。静脉注射Ang-（1-7）（55 pmol / min，静脉内）增强了全身动脉压的降低。注射BK和BK类似物[Hyp3，Tyr（Me）8]-缓激肽（HT-BK）和[Phe8psi（CH2-NH）Arg9]-缓激肽（PA-BK），而不会改变对Ang I或II的升压反应，或对乙酰胆碱和硝普钠的降压药反应。血管紧张素转换酶（ACE）抑制剂依那普利拉增强了对BK和BK类似物HT-BK的响应，而没有改变对PA-BK的响应并抑制了对Ang I的响应。Ang-（1-7）和依那普利对响应的增强作用Ang-（1-7）受体拮抗剂A-779不会减弱BK的毒性。 Ang-（1-7）-和ACE抑制剂对BK的增强反应被BK B2受体拮抗剂Hoe 140减弱。环氧合酶抑制剂甲氯芬酸钠对BK或Ang-（1-7）-增强的反应无明显影响BK回应。这些结果表明，Ang-（1-7）通过选择性B2受体机制增强了对BK的反应，该机制独立于对Ang-（1-7）受体，ACE或环氧合酶产物形成的影响。这些数据表明，ACE抑制剂对BK的增强反应不是由A-779敏感机制介导的，并且与依那普利拉诱导的BK增强作用归因于BK失活减少的假设相一致。

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