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Postjunctional alpha(2C)-adrenoceptor contractility in human saphenous vein.

C A Rizzo1, L M Ruck, M R Corboz

  • 1Schering-Plough Research Institute, Allergy, K-15-1-1600, 2015 Galloping Hill Road, Kenilworth, NJ 07033, USA. charles.rizzo@spcorp.com

European Journal of Pharmacology
|February 28, 2001
PubMed
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Human saphenous vein contracts via alpha(2)-adrenoceptors, primarily the alpha(2C) subtype. Both alpha(1)- and alpha(2)-adrenoceptors contribute to vein contractions, with alpha(2C) being the dominant postjunctional receptor.

Area of Science:

  • Pharmacology
  • Vascular Biology
  • Adrenoceptor Research

Background:

  • Postjunctional alpha(2)-adrenoceptors mediate contractility in various tissues.
  • The specific alpha(2)-adrenoceptor subtype responsible for contractility in human saphenous veins remains to be fully elucidated.

Purpose of the Study:

  • To characterize the postjunctional alpha(2)-adrenoceptor-mediated contractility in human saphenous vein.
  • To identify the predominant alpha(2)-adrenoceptor subtype involved in human saphenous vein contractions.

Main Methods:

  • Human saphenous vein segments were used for contractility studies.
  • Selective alpha(2)-adrenoceptor agonists (BHT-920, UK 14,304) and antagonists (yohimbine, ARC 239, WB 4101, HV 723) were employed.
  • Recombinant human alpha(2A)-, alpha(2B)-, and alpha(2C)-adrenoceptor competition binding assays were performed.

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Main Results:

  • Human saphenous vein exhibited concentration-dependent contractions to alpha(2)-adrenoceptor selective agonists.
  • Yohimbine selectively inhibited agonist-induced contractions, while prazosin did not.
  • Binding assays revealed a higher affinity for yohimbine and WB 4101 at the alpha(2C)-adrenoceptor subtype.

Conclusions:

  • Both alpha(1)- and alpha(2)-adrenoceptors can elicit contractions in human saphenous vein.
  • The alpha(2C)-adrenoceptor is the predominant postjunctional alpha(2)-adrenoceptor subtype in human saphenous vein.
  • These findings contribute to understanding vascular adrenergic signaling.