Modulation of ACh-induced currents in rat adrenal chromaffin cells by ligands of α2 adrenergic and imidazoline receptors

Mamoru Takeda, Jacqueline K. Phillips, Ratna Dubey, Jaimie W. Polson, Janusz Lipski*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

12 Citations (Scopus)


The aim of this study was to investigate the expression of the α2-adrenergic receptors in the adrenal medulla, and to examine the mechanism by which clonidine and related drugs inhibit acetylcholine (ACh)-induced whole-cell currents in adrenal chromaffin cells. Reverse transcription-polymerase chain reaction (RT-PCR) performed on punches of rat adrenal medulla demonstrated expression of mRNA for the α2A-, α2B- and α2C-adrenergic receptors. Similar experiments conducted with tissue punches obtained from the adrenal cortex did not reveal expression of these receptor subtypes. Whole-cell currents were recorded in isolated chromaffin cells using the perforated-patch configuration. ACh (50 μM) evoked inward currents with a peak amplitude of 117.8±9.3 pA (n=45; Vhol=-60 mV). The currents were inhibited in a dose-dependent manner (0.5-50 μM) by clonidine, UK 14,304 and rilmenidine (agonists of α2/imidazoline receptors), as well as by SKF 86466 and efaroxan (antagonists). Adrenaline and noradrenaline (50-100 μM) had no significant effect. Thus, although the adrenal medulla expresses mRNA for the α2-adrenergic receptors, the lack of agonist-antagonist specificity observed in our whole-cell recordings (in the absence of intracellular dialysis) provides additional evidence against the possibility that these inhibitory effects are mediated by classical α2 or imidazoline receptor interactions.

Original languageEnglish
Pages (from-to)151-159
Number of pages9
JournalAutonomic Neuroscience: Basic and Clinical
Issue number3
Publication statusPublished - 14 May 2001
Externally publishedYes


  • Adrenal glands
  • Catecholamines
  • Dissociated chromaffin cells
  • Electrophysiology
  • Rat
  • RT-PCR


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