Modulation of ACh-induced currents in rat adrenal chromaffin cells by ligands of α2 adrenergic and imidazoline receptors
| Autor: | Janusz Lipski, Jaimie W. Polson, Jacqueline K. Phillips, Ratna Dubey, Mamoru Takeda |
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| Rok vydání: | 2001 |
| Předmět: |
Male
medicine.medical_specialty Adrenergic receptor Chromaffin Cells Receptors Drug Gene Expression Imidazoline receptor Ligands Cellular and Molecular Neuroscience chemistry.chemical_compound Catecholamines Internal medicine Adrenal Glands medicine Animals Rats Wistar Receptor Adrenergic alpha-Antagonists Endocrine and Autonomic Systems Chemistry Electric Conductivity Receptors Adrenergic alpha Efaroxan Acetylcholine Rilmenidine Enzymes Rats Electrophysiology medicine.anatomical_structure Endocrinology Chromaffin cell Catecholamine Female Imidazoline Receptors Neurology (clinical) Adrenal medulla Adrenergic alpha-Agonists medicine.drug |
| Zdroj: | Autonomic Neuroscience. 88:151-159 |
| ISSN: | 1566-0702 |
| DOI: | 10.1016/s1566-0702(01)00221-1 |
| Popis: | The aim of this study was to investigate the expression of the alpha2-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 2A-, alpha2B- and alpha2C-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 microM) 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 microM) by clonidine, UK 14,304 and rilmenidine (agonists of alpha2/imidazoline receptors), as well as by SKF 86466 and efaroxan (antagonists). Adrenaline and noradrenaline (50-100 microM) had no significant effect. Thus, although the adrenal medulla expresses mRNA for the alpha2-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 alpha2 or imidazoline receptor interactions. |
| Databáze: | OpenAIRE |
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