Rat vena cava alpha 1B-adrenoceptors: characterization by [3H]prazosin binding and contraction experiments

Eur J Pharmacol. 1993 Aug 15;246(3):275-81. doi: 10.1016/0922-4106(93)90042-8.


We examined which subtypes of alpha 1-adrenoceptors are expressed in rat vena cava by using both functional and [3H]prazosin binding experiments. Pretreatment with chloroethylclonidine inactivated about 80% of the specific [3H]prazosin binding sites and reduced the maximal noradrenaline-induced contraction to the same extent. Competition with subtype-selective agonists and antagonists showed primarily the alpha 1B-adrenoceptor subtype in vena cava. The number of alpha 1-adrenoceptors estimated with [3H]prazosin binding and the maximal noradrenaline-induced contraction were dose-dependently inhibited by phenoxybenzamine, indicating the absence of receptor reserve for noradrenaline in vena cava. As the noradrenaline-induced contraction was largely inhibited in Ca(2+)-free solution, these results suggest that alpha 1B-adrenoceptors can be mainly linked to Ca2+ influx in rat vena cava.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • In Vitro Techniques
  • Norepinephrine / pharmacology
  • Prazosin / metabolism*
  • Radioligand Assay
  • Rats
  • Receptors, Adrenergic, alpha-1 / metabolism*
  • Tritium
  • Vasoconstriction / drug effects*
  • Venae Cavae / drug effects*
  • Venae Cavae / metabolism
  • Venae Cavae / physiology


  • Receptors, Adrenergic, alpha-1
  • Tritium
  • Norepinephrine
  • Prazosin