Almeida A P, Frábregas B C, Madureira M M, Santos R J, Campagnole-Santos M J, Santos R A
Departamento de Fisiologia e Biofísica, Universidade Federal de Minas Gerais, Belo Horizonte, MG, Brasil.
Braz J Med Biol Res. 2000 Jun;33(6):709-13. doi: 10.1590/s0100-879x2000000600012.
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.
已有研究表明，在清醒大鼠中输注血管紧张素 -（1 - 7）（Ang -（1 - 7））可增强缓激肽（BK）诱导的降压反应。本研究旨在确定在按照Langendorff技术灌注的离体大鼠心脏中Ang -（1 - 7）与BK的相互作用。切除心脏并通过主动脉残端以恒定流量用Krebs - Ringer溶液灌注，记录灌注压力和心脏收缩力的变化。静脉注射BK（2.5、5、10和20 ng）产生剂量依赖性降压作用。向灌注液中添加Ang -（1 - 7）（2 ng/ml）不会改变灌注压力或收缩力，但会使较低剂量BK的降压作用加倍。BK增强Ang -（1 - 7）的活性可被吲哚美辛（5 mg/kg，腹腔注射）或L - NAME（30 mg/kg，腹腔注射）预处理所阻断。Ang -（1 - 7）拮抗剂A - 779（在Krebs - Ringer中为50 ng/ml）完全阻断了Ang -（1 - 7）对BK诱导的血管舒张的作用。这些数据表明，Ang -（1 - 7）对BK诱导的血管舒张的增强作用可归因于通过Ang -（1 - 7）受体介导的机制释放一氧化氮和血管舒张性前列腺素。
