Summary
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1.
Effects of imidazole compounds and guanabenz on the stimulus-evoked release of catecholamine (CA) were studied in cultured bovine adrenal chromaffin cells.
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2.
Clonidine, oxymetazoline, phentolamine, chlorpheniramine, and guanabenz inhibited acetylcholine (ACh)-evoked CA release in a dose-dependent manner, but not high K+-evoked release.
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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.
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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.
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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.
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Ohara-Imaizumi, M., Kumakura, K. Effects of imidazole compounds on catecholamine release in adrenal chromaffin cells. Cell Mol Neurobiol 12, 273–283 (1992). https://doi.org/10.1007/BF00712931
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DOI: https://doi.org/10.1007/BF00712931