Angiotensin-(1-7) potentiates the coronary vasodilatatory effect of bradykinin in the isolated rat heart
Angiotensin-(1-7) potentiates the coronary vasodilatatory effect of bradykinin in the isolated rat heart
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DOI：
10.1590/s0100-879x2000000600012
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发表时间：
2000-06-01
影响因子：
2.3
通讯作者：
Santos, RAS
中科院分区：
文献类型：
--
作者：
Almeida, AP;Frábregas, BC;Santos, RAS
研究表明，血管紧张素-（1-7）（Ang-（1-7））灌注增强缓激肽（BK）诱导的清醒大鼠舒张反应。本研究采用Langendorff灌流技术，观察了Ang-（1-7）-BK相互作用。离体心脏经主动脉残端灌注Krebs-Ringer液，记录灌注压和心脏收缩力的变化。大剂量注射BK（2.5、5、10和20 ng）产生剂量依赖性的肿胀效应。灌流液中加入Ang-（1-7）（2 ng/ml）并不改变灌流压或收缩力，但可使低剂量BK的收缩作用加倍。Ang-（1-7）拮抗剂A-779（50 ng/ml）可完全阻断Ang-（1 - 7）对BK诱导的血管舒张作用。这些数据表明，Ang（1-7）增强BK诱导的血管舒张作用可归因于通过Ang-（1 -7）受体介导的机制释放一氧化氮和血管舒张剂胰高血糖素。
It has been shown that angiotensin-(1-7) (Ang-(1-7)) infusion potentiates the bradykinin (BK)-induced hypotensive response in conscious rats, The present study was conducted to identify Ang-(1-7)-BK interactions in the isolated rat heart perfused according to the Langendorff technique, Hearts were excised and perfused through the aortic stump under a constant flow with Krebs-Ringer solution and the changes in perfusion pressure and heart contractile force were recorded. Bolus injections of BK (2.5, 5, 10 and 20 ng) produced a dose-dependent hypotensive effect. Ang-(1-7) added to the perfusion solution (2 ng/ml) did not change the perfusion pressure or the contractile force but doubled the hypotensive effect of the lower doses of BK. The BK-potentiating Ang-(1-7) activity was blocked by pretreatment with indomethacin (5 mg/kg, ip) or L-NAME (30 mg/kg, ip), The Ang-(1-7) antagonist A-779 (50 ng/ml in Krebs-Ringer) completely blocked the effect of Ang-(1-7) on BK-induced vasodilation. These data suggest that the potentiation of the BK-induced vasodilation by Ang(1-7) can be attributed to the release of nitric oxide and vasodilator prostaglandins through an Ang-(1-7) receptor-mediated mechanism.