The Effects of Angiotensin II or Angiotensin 1-7 on Rat Pial Microcirculation during Hypoperfusion and Reperfusion Injury: Role of Redox Stress
Renin–angiotensin systems produce angiotensin II (Ang II) and angiotensin 1-7 (Ang 1-7), which are able to induce opposite effects on circulation. This study in vivo assessed the effects induced by Ang II or Ang 1-7 on rat pial microcirculation during hypoperfusion–reperfusion, clarifying the mechan...
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MDPI AG
2021-12-01
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author | Dominga Lapi Maurizio Cammalleri Massimo Dal Monte Martina Di Maro Mariarosaria Santillo Anna Belfiore Gilda Nasti Simona Damiano Rossella Trio Martina Chiurazzi Barbara De Conno Nicola Serao Paolo Mondola Antonio Colantuoni Bruna Guida |
author_facet | Dominga Lapi Maurizio Cammalleri Massimo Dal Monte Martina Di Maro Mariarosaria Santillo Anna Belfiore Gilda Nasti Simona Damiano Rossella Trio Martina Chiurazzi Barbara De Conno Nicola Serao Paolo Mondola Antonio Colantuoni Bruna Guida |
author_sort | Dominga Lapi |
collection | DOAJ |
description | Renin–angiotensin systems produce angiotensin II (Ang II) and angiotensin 1-7 (Ang 1-7), which are able to induce opposite effects on circulation. This study in vivo assessed the effects induced by Ang II or Ang 1-7 on rat pial microcirculation during hypoperfusion–reperfusion, clarifying the mechanisms causing the imbalance between Ang II and Ang 1-7. The fluorescence microscopy was used to quantify the microvascular parameters. Hypoperfusion and reperfusion caused vasoconstriction, disruption of blood–brain barrier, reduction of capillary perfusion and an increase in reactive oxygen species production. Rats treated with Ang II showed exacerbated microvascular damage with stronger vasoconstriction compared to hypoperfused rats, a further increase in leakage, higher decrease in capillary perfusion and marker oxidative stress. Candesartan cilexetil (specific Ang II type 1 receptor (AT<sub>1</sub>R) antagonist) administration prior to Ang II prevented the effects induced by Ang II, blunting the hypoperfusion–reperfusion injury. Ang 1-7 or ACE2 activator administration, preserved the pial microcirculation from hypoperfusion–reperfusion damage. These effects of Ang 1-7 were blunted by a Mas (Mas oncogene-encoded protein) receptor antagonist, while Ang II type 2 receptor antagonists did not affect Ang 1-7-induced changes. In conclusion, Ang II and Ang 1-7 triggered different mechanisms through AT<sub>1</sub>R or MAS receptors able to affect cerebral microvascular injury. |
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language | English |
last_indexed | 2024-03-10T04:32:31Z |
publishDate | 2021-12-01 |
publisher | MDPI AG |
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series | Biomolecules |
spelling | doaj.art-2789f326f70f4ad99801316d265aa9232023-11-23T04:00:20ZengMDPI AGBiomolecules2218-273X2021-12-011112186110.3390/biom11121861The Effects of Angiotensin II or Angiotensin 1-7 on Rat Pial Microcirculation during Hypoperfusion and Reperfusion Injury: Role of Redox StressDominga Lapi0Maurizio Cammalleri1Massimo Dal Monte2Martina Di Maro3Mariarosaria Santillo4Anna Belfiore5Gilda Nasti6Simona Damiano7Rossella Trio8Martina Chiurazzi9Barbara De Conno10Nicola Serao11Paolo Mondola12Antonio Colantuoni13Bruna Guida14Department of Biology, University of Pisa, Via San Zeno, 31, 56127 Pisa, ItalyDepartment of Biology, University of Pisa, Via San Zeno, 31, 56127 Pisa, ItalyDepartment of Biology, University of Pisa, Via San Zeno, 31, 56127 Pisa, ItalyDepartment of Clinical Medicine and Surgery, Federico II University of Naples, Via S. Pansini, 5, 80131 Naples, ItalyDepartment of Clinical Medicine and Surgery, Federico II University of Naples, Via S. Pansini, 5, 80131 Naples, ItalyDepartment of Clinical Medicine and Surgery, Federico II University of Naples, Via S. Pansini, 5, 80131 Naples, ItalyDepartment of Clinical Medicine and Surgery, Federico II University of Naples, Via S. Pansini, 5, 80131 Naples, ItalyDepartment of Clinical Medicine and Surgery, Federico II University of Naples, Via S. Pansini, 5, 80131 Naples, ItalyDepartment of Clinical Medicine and Surgery, Federico II University of Naples, Via S. Pansini, 5, 80131 Naples, ItalyDepartment of Clinical Medicine and Surgery, Federico II University of Naples, Via S. Pansini, 5, 80131 Naples, ItalyDepartment of Clinical Medicine and Surgery, Federico II University of Naples, Via S. Pansini, 5, 80131 Naples, ItalyDepartment of Clinical Medicine and Surgery, Federico II University of Naples, Via S. Pansini, 5, 80131 Naples, ItalyDepartment of Clinical Medicine and Surgery, Federico II University of Naples, Via S. Pansini, 5, 80131 Naples, ItalyDepartment of Clinical Medicine and Surgery, Federico II University of Naples, Via S. Pansini, 5, 80131 Naples, ItalyDepartment of Clinical Medicine and Surgery, Federico II University of Naples, Via S. Pansini, 5, 80131 Naples, ItalyRenin–angiotensin systems produce angiotensin II (Ang II) and angiotensin 1-7 (Ang 1-7), which are able to induce opposite effects on circulation. This study in vivo assessed the effects induced by Ang II or Ang 1-7 on rat pial microcirculation during hypoperfusion–reperfusion, clarifying the mechanisms causing the imbalance between Ang II and Ang 1-7. The fluorescence microscopy was used to quantify the microvascular parameters. Hypoperfusion and reperfusion caused vasoconstriction, disruption of blood–brain barrier, reduction of capillary perfusion and an increase in reactive oxygen species production. Rats treated with Ang II showed exacerbated microvascular damage with stronger vasoconstriction compared to hypoperfused rats, a further increase in leakage, higher decrease in capillary perfusion and marker oxidative stress. Candesartan cilexetil (specific Ang II type 1 receptor (AT<sub>1</sub>R) antagonist) administration prior to Ang II prevented the effects induced by Ang II, blunting the hypoperfusion–reperfusion injury. Ang 1-7 or ACE2 activator administration, preserved the pial microcirculation from hypoperfusion–reperfusion damage. These effects of Ang 1-7 were blunted by a Mas (Mas oncogene-encoded protein) receptor antagonist, while Ang II type 2 receptor antagonists did not affect Ang 1-7-induced changes. In conclusion, Ang II and Ang 1-7 triggered different mechanisms through AT<sub>1</sub>R or MAS receptors able to affect cerebral microvascular injury.https://www.mdpi.com/2218-273X/11/12/1861cerebral microcirculationrenin–angiotensin systemhypoperfusion–reperfusionangiotensin IIangiotensin-1-7 |
spellingShingle | Dominga Lapi Maurizio Cammalleri Massimo Dal Monte Martina Di Maro Mariarosaria Santillo Anna Belfiore Gilda Nasti Simona Damiano Rossella Trio Martina Chiurazzi Barbara De Conno Nicola Serao Paolo Mondola Antonio Colantuoni Bruna Guida The Effects of Angiotensin II or Angiotensin 1-7 on Rat Pial Microcirculation during Hypoperfusion and Reperfusion Injury: Role of Redox Stress Biomolecules cerebral microcirculation renin–angiotensin system hypoperfusion–reperfusion angiotensin II angiotensin-1-7 |
title | The Effects of Angiotensin II or Angiotensin 1-7 on Rat Pial Microcirculation during Hypoperfusion and Reperfusion Injury: Role of Redox Stress |
title_full | The Effects of Angiotensin II or Angiotensin 1-7 on Rat Pial Microcirculation during Hypoperfusion and Reperfusion Injury: Role of Redox Stress |
title_fullStr | The Effects of Angiotensin II or Angiotensin 1-7 on Rat Pial Microcirculation during Hypoperfusion and Reperfusion Injury: Role of Redox Stress |
title_full_unstemmed | The Effects of Angiotensin II or Angiotensin 1-7 on Rat Pial Microcirculation during Hypoperfusion and Reperfusion Injury: Role of Redox Stress |
title_short | The Effects of Angiotensin II or Angiotensin 1-7 on Rat Pial Microcirculation during Hypoperfusion and Reperfusion Injury: Role of Redox Stress |
title_sort | effects of angiotensin ii or angiotensin 1 7 on rat pial microcirculation during hypoperfusion and reperfusion injury role of redox stress |
topic | cerebral microcirculation renin–angiotensin system hypoperfusion–reperfusion angiotensin II angiotensin-1-7 |
url | https://www.mdpi.com/2218-273X/11/12/1861 |
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