Patients who develop vasodilatory shock, particularly when caused by an inflammatory condition like sepsis or pancreatitis, have evidence of significant endothelial injury as manifested by coagulation disorders and increased capillary permeability. Endothelial injury during shock may lead to ACE defects, which in turn may cause an increase in vasodilatory mediators that are normally metabolized by ACE and a relative or absolute decrease in ANG-2. These pathophysiological derangements may be beneficially affected by ANG-2 infusion. This mechanism of action in shock justifies further investigation of ACE activity, bradykinin levels, and ANG 1-7 levels in vasodilatory shock and may be an important target for future therapeutic intervention.

Read More