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Angiotensin-(1-7) improves the post-ischemic function in isolated perfused rat hearts
A J Ferreira1, R A S Santos, A P Almeida
1Laboratório de Hipertensão, Departamento de Fisiologia e Biofísica, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, MG, Brasil.
Summary
Angiotensin-(1-7) (Ang-(1-7)) significantly improves heart function after ischemia and reperfusion in rat hearts. This protective effect is mediated by bradykinin and prostaglandins, highlighting Ang-(1-7) as a potential therapeutic agent for cardiac injury.
Area of Science:
- Cardiovascular Physiology
- Renal Physiology
- Pharmacology
Background:
- The renin-angiotensin system plays a crucial role in cardiovascular regulation.
- Angiotensin-(1-7) (Ang-(1-7)) is a bioactive peptide with known cardiovascular effects.
- Ischemia-reperfusion injury is a major cause of myocardial damage.
Purpose of the Study:
- To evaluate the protective effects of Ang-(1-7) on post-ischemic cardiac function.
- To investigate the underlying mechanisms of Ang-(1-7)-mediated cardioprotection.
Main Methods:
- Isolated adult male Wistar rat hearts were perfused using the Langendorff technique.
- Myocardial ischemia was induced by coronary ligation (15 min), followed by reperfusion (30 min).
- Hearts were treated with Ang-(1-7), Angiotensin II (Ang II), or specific antagonists (A-779, HOE 140, indomethacin, L-NAME).
Main Results:
- Ang-(1-7) (0.22 nM) prevented the reduction in systolic tension during reperfusion after ischemia.
- Ang II did not offer the same protective effect.
- The cardioprotective effect of Ang-(1-7) was blocked by A-779 and HOE 140, and indomethacin, but not L-NAME.
Conclusions:
- Low-concentration Ang-(1-7) significantly improves myocardial systolic tension following ischemia-reperfusion.
- The protective mechanism involves Ang-(1-7) receptors, bradykinin B2 receptors, and prostaglandin release.
- Ang-(1-7) demonstrates potential as a therapeutic agent for mitigating cardiac ischemia-reperfusion injury.