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Related Experiment Videos

ACE insertion/deletion genotype affects bradykinin metabolism

N J Brown1, C Blais, S K Gandhi

  • 1Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee 37232-6602, USA.

Journal of Cardiovascular Pharmacology
|September 11, 1998
PubMed
Summary

The angiotensin-converting enzyme (ACE) deletion allele enhances bradykinin breakdown. This suggests a new pathway linking the ACE D allele to negative cardiovascular outcomes.

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Area of Science:

  • Cardiovascular Genetics
  • Enzymology
  • Pharmacogenomics

Background:

  • The angiotensin-converting enzyme (ACE) deletion allele is linked to cardiovascular issues.
  • ACE activity influences angiotensin (Ang) I to Ang II conversion.
  • Bradykinin is a peptide that protects the cardiovascular system.

Purpose of the Study:

  • To investigate the association between the ACE deletion allele and bradykinin degradation.
  • To determine if ACE genotype affects bradykinin metabolism.

Main Methods:

  • Measured synthetic bradykinin metabolism in serum from individuals with ACE deletion (DD) or insertion (II) alleles.
  • Subjects underwent an Angiotensin I infusion protocol.
  • Analyzed serum ACE activity, Ang II concentrations, and bradykinin half-life.

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Main Results:

  • ACE DD subjects showed a trend towards higher ACE levels compared to II subjects.
  • Plasma Ang II concentrations were elevated in DD subjects during Ang I infusion.
  • Bradykinin half-life was significantly shorter in DD subjects (26.3 s) versus II subjects (42.1 s).
  • Inverse relationships were found between bradykinin half-life and ACE activity/Ang I to Ang II conversion.

Conclusions:

  • ACE genotype significantly influences bradykinin degradation rates.
  • Enhanced bradykinin breakdown by the ACE D allele may contribute to cardiovascular risks.