Published Feb 26, 2016
WithAnyLuck20
3 Posts
Is anyone willing to explain the pathophysiology of this? It would be much appreciated!
Wile E Coyote, ASN, RN
471 Posts
What has your own research shown you?
Well if the research was cohesive enough for me to understand it I wouldn't ask
That's not how this works. Generally speaking, we prefer teaching a person to fish over just feeding them. Hence the many views with only my response thus far.
Rocknurse, MSN, APRN, NP
1,367 Posts
The etiology of ACE inhibitor-induced angioedema is unknown but it is likely caused by the increase in bradykinin. Bradykinin is an inflammatory peptide that has a vasoactive property and causes vasodilation. The vasodilation would in turn cause the angioedema due to congestion in the vessels.
Explaining this simply, ACE inhibitors work by preventing the conversion of Angiotensin I to Angiotensin II. The two enzymes are responsible for vasocontriction. The premise behind ACE inhibitors is to lower blood pressure by blocking this mechanism, dilating the essels and reducing pressure. Because Angiotensin II is responsible for inactivating bradykinin, blocking Angiotensin II will also block inactivation of bradykinin, leading to angioedema. Hope that helps.