Use of transgenic (knockout) mice reveals a site distinct from the alpha2A-adrenoceptors for agmatine in the vas deferens

Pharmacol Rep. 2009 Mar-Apr;61(2):325-9. doi: 10.1016/s1734-1140(09)70039-8.

Abstract

The inhibitory effect of agmatine on electrically induced contractions was studied in vas deferens of Adra 2a transgenic mice lacking alpha(2A)-adrenoceptors. Agmatine and clonidine caused a concentration-dependent inhibition of twitches. However, while agmatine showed a similar pIC(50) value in control and transgenic mice, the pIC(50) value for clonidine was about 30-fold lower in knockout mice. In both strains, yohimbine shifted the curve for clonidine, but not for agmatine, even when a 100-fold higher concentration of yohimbine was employed. Our results indicate that inhibition by agmatine in mouse vas deferens is not simply due to interactions with alpha(2)-adrenoceptors in our experimental conditions.

MeSH terms

  • Agmatine / pharmacology*
  • Animals
  • Clonidine / pharmacology
  • Dose-Response Relationship, Drug
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Mice, Transgenic
  • Muscle Contraction / drug effects
  • Receptors, Adrenergic, alpha-2 / drug effects
  • Receptors, Adrenergic, alpha-2 / physiology*
  • Vas Deferens / drug effects*
  • Vas Deferens / physiology

Substances

  • Adra2a protein, mouse
  • Receptors, Adrenergic, alpha-2
  • Agmatine
  • Clonidine