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Alpha-2B adrenoceptor polymorphism and peripheral vasoconstriction.

Pekka Talke1, Claudia Stapelfeldt, Errol Lobo

  • 1Department of Anesthesia and Perioperative Medicine, University of California, San Francisco, California 94143-0648, USA. talkep@anesthesia.ucsf.edu

Pharmacogenetics and Genomics
|May 3, 2005
PubMed
Summary
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Individuals with the alpha-2B adrenoceptor DD genotype experienced enhanced vasoconstriction initially upon receiving dexmedetomidine. This heightened vasoconstrictive response was temporary and not sustained throughout the infusion.

Area of Science:

  • Pharmacology
  • Genetics
  • Cardiovascular Physiology

Background:

  • Alpha-2B adrenoceptors (AR) mediate vasoconstriction.
  • A deletion variant (D) in the human alpha-2B AR is linked to reduced receptor desensitization.
  • This may result in exaggerated vasoconstriction following alpha-2 AR activation.

Purpose of the Study:

  • To investigate if alpha-2 AR activation causes enhanced vasoconstriction in individuals with the alpha-2B AR DD genotype compared to II or DI genotypes.
  • To test the hypothesis of genotype-dependent vasoconstrictive responses to alpha-2 agonists.

Main Methods:

  • Intravenous administration of dexmedetomidine (an alpha-2 agonist) to 80 surgical patients under general anesthesia.
  • Measurement of finger blood volume via photoplethysmography (finger LTF) as an indicator of vasoconstriction.

Related Experiment Videos

  • Monitoring of hemodynamic variables.

    • Main Results:

    • Dexmedetomidine induced vasoconstriction (increased LTF), increased systolic blood pressure, and decreased heart rate in all genotype groups.
    • The increase in LTF was significantly more pronounced in the DD genotype group at 3 minutes post-infusion (P=0.014).
    • No significant differences in LTF, blood pressure, or heart rate were observed between groups later in the infusion or post-infusion.

    Conclusions:

    • Dexmedetomidine reliably induces peripheral vasoconstriction.
    • The alpha-2B DD genotype is associated with an initial enhanced vasoconstrictive response to dexmedetomidine.
    • This enhanced response is transient and not sustained during or after the infusion period.