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. 1992 Jun;12(3):273–283. doi: 10.1007/BF00712931

Effects of imidazole compounds on catecholamine release in adrenal chromaffin cells

Mica Ohara-Imaizumi 1, Konosuke Kumakura 1,✉
PMCID: PMC11567360  PMID: 1330311

Abstract

  1. Effects of imidazole compounds and guanabenz on the stimulus-evoked release of catecholamine (CA) were studied in cultured bovine adrenal chromaffin cells.

  2. Clonidine, oxymetazoline, phentolamine, chlorpheniramine, and guanabenz inhibited acetylcholine (ACh)-evoked CA release in a dose-dependent manner, but not high K+-evoked release.

  3. The inhibition by these compounds was not antagonized by nonimidazole and nonguanidineα 2-antagonists (yohimbine and phenoxybenzamine) but was significantly antagonized by tolazoline (imidazoleα 2-antagonist) and cimetidine (imidazole H2-antagonist). Moreover, tolazoline by itself augmented the ACh-evoked, but not the high K+-evoked, CA release.

  4. Although chlorpheniramine and cimetidine are antagonists for H1 and H2 histaminergic receptors, the site of action for these compounds in our results seemed to differ from the histamine receptors.

  5. These results suggest that the inhibitory action of imidazole compounds and guanabenz on ACh-evoked CA release in adrenal chromaffin cells is mediated through an imidazole receptor. Adrenal chromaffin cells may contain an endogenous clonidine-displacing substance (CDS) which has been found in adrenal gland and brain as an endogenous ligand for imidazole receptors. Thus, CDS may have a regulatory role in the stimulus-secretion coupling in these cells.

Key words: chromaffin cells, catecholamine release, imidazole compounds, clonidine, guanabenz, imidazole receptor

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