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At high levels of Ang-II (left), increased binding of Ang-II to AT1R enhances availability of ACE2 to the invading virus. Conversely, low levels of Ang-II (right) frees AT1R to form complexes with ACE2 (dashed green lines) that increase conversion of Ang-II to Ang(1–7) and decrease interaction of the virus with ACE2.
