Abstract
Introduction:
ACE2 alternatively converts angiotensin (Ang) II into Ang-(1–7) and Ang I into Ang-(1–9). There is little information in the literature with respect to Ang-(1–9) properties. A number of studies show a link between peptides of the renin-angiotensin system and thrombosis.
Materials and methods:
We have investigated the influence of Ang-(1–9) on stasis-induced venous thrombosis in the rat. The contribution of coagulation and fibrinolytic systems, angiotensin receptor type 1 (AT1) and MAS receptor in the mode of Ang-(1–9) action was also determined.
Results:
Ang-(1–9) enhanced thrombosis development, decreased plasma concentration of tissue plasminogen activator and increased the level of its inhibitor (PAI-1). The action of Ang-(1–9) was reversed by selective antagonist of AT1 receptor, but not Ang-(1–7) antagonist. Ang-(1–9) did not bind to the AT1 receptor.
Conclusions:
Ang-(1–9) enhances venous thrombosis in the rat because of the impairment of fibrinolysis. The prothrombotic effect of Ang-(1–9) is mediated by Ang II acting via the AT1 receptor.
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