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The antithrombotic effect of angiotensin-(1-7) involves mas-mediated NO release from platelets

Rodrigo Araújo Fraga-Silva1, Sergio Veloso Brant Pinheiro, Andrey Christian Costa Gonçalves

  • 1Department of Physiology, Federal University of Minas Gerais, Belo Horizonte, Minas Gerais, Brazil.

Molecular Medicine (Cambridge, Mass.)
|November 21, 2007
PubMed

Insights

Angiotensin-(1-7) has an antithrombotic effect mediated by the Mas receptor in platelets, involving nitric oxide release. This Mas-dependent mechanism is crucial for preventing thrombus formation and regulating hemostasis.

Area of Science:

  • Cardiovascular Biology
  • Hemostasis and Thrombosis
  • Molecular Pharmacology

Background:

  • The antithrombotic effects of Angiotensin-(1-7) [Ang-(1-7)] are known, but the underlying mechanisms, particularly platelet involvement and Mas receptor signaling, remain unclear.
  • Understanding these pathways is crucial for developing novel antithrombotic therapies.

Purpose of the Study:

  • To investigate the role of platelets and the Mas receptor in the antithrombotic action of Ang-(1-7).
  • To elucidate the mechanism of Ang-(1-7)-induced nitric oxide (NO) release from platelets.
  • To determine the in vivo relevance of Mas in Ang-(1-7)-mediated antithrombosis and hemostasis.

Main Methods:

  • Western blotting to detect Mas protein in rat platelets.
  • Fluorescent binding assays using FAM-Ang-(1-7) and Mas antagonist A-779 in rat and mouse platelets (Mas(-/-) and Mas(+/+)).
  • Measurement of NO release using DAF-FM indicator.
  • In vivo assessment of thrombus formation in mouse vena cava and bleeding time in Mas(+/+) and Mas(-/-) mice.

Main Results:

  • Mas protein and specific Ang-(1-7) binding were identified in rat and mouse platelets, dependent on the Mas receptor.
  • Ang-(1-7) stimulated NO release from platelets, an effect blocked by A-779 and absent in Mas(-/-) platelets.
  • Ang-(1-7) inhibited thrombus formation in Mas(+/+) mice, but this effect was abolished in Mas(-/-) mice.
  • Mas deficiency significantly reduced bleeding time, indicating impaired hemostasis.

Conclusions:

  • This study provides the first evidence for Mas protein and Ang-(1-7) binding in platelets.
  • The antithrombotic effect of Ang-(1-7) is mediated through Mas-dependent NO release from platelets.
  • Mas receptor signaling is essential for the in vivo antithrombotic efficacy of Ang-(1-7) and plays a critical role in hemostasis.

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