Interestingly, ACE has a higher affinity for BDK [24] and therefore in conditions where ACE is low, the vasopressor system is moved toward a BDK-directed hypotensive axis. BDK takes part in the inflammatory response after injury and acts to induce pain via stimulation of the BDKRB1 receptor, which also causes neutrophil recruitment and a major vascular permeability [25, 26].