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Plasma bradykinin in angio-oedema
J Nussberger1, M Cugno, C Amstutz
1Hypertension Division, University Hospital Lausanne, Switzerland.
Lancet (London, England)
|September 12, 1998
Summary
Plasma bradykinin levels increase significantly during angio-oedema attacks in hereditary and acquired conditions, as well as with ACE inhibitor use. This study developed a reliable assay to measure bradykinin, confirming its role in angio-oedema pathogenesis.
Area of Science:
- Biochemistry
- Immunology
- Pharmacology
Background:
- Bradykinin is implicated as a key mediator in hereditary angio-oedema (HA), acquired angio-oedema (AA), and ACE inhibitor-induced angio-oedema.
- Previous measurement challenges hindered definitive proof of bradykinin's role in these conditions.
Purpose of the Study:
- To develop and utilize a reliable assay for measuring plasma bradykinin concentrations.
- To investigate plasma bradykinin levels in patients with HA, AA, and ACE inhibitor-induced angio-oedema during attacks and remission.
Main Methods:
- A specific assay combining liquid-phase extraction, high-performance liquid chromatography, and radioimmunoassay (RIA) was employed.
- Plasma bradykinin was measured in healthy volunteers, patients with HA and AA, and a patient on ACE inhibitors.
Main Results:
- Plasma bradykinin concentrations decreased with age in healthy individuals.
- Bradykinin levels were elevated in patients with AA and showed substantial increases during acute attacks of HA, AA, and captopril-induced angio-oedema.
- Infusion of C1-esterase inhibitor normalized bradykinin levels in HA and AA patients; drug withdrawal normalized levels in the ACE inhibitor patient.
Conclusions:
- The developed assay confirms elevated plasma bradykinin during acute angio-oedema episodes across different etiologies.
- Bradykinin's role as a mediator in angio-oedema is further substantiated, with potential therapeutic implications for C1-esterase inhibitor and ACE inhibitor management.