Effect of repeated administration of clonidine on adrenergic, cholinergic (muscarinic), dopaminergic, and serotonergic receptors in brain regions of rats

Clonidine (0.1 mg/kg) or its vehicle was administered orally to rats for 2 months. A significant decrease in mean blood pressure was observed in clonidine treated rats. Chronic administration of clonidine in rats produced alterations in central receptors. In hypothalamus and medulla, clonidine in treatment increased the Bmax value of 3H‐dihydroergocryptine binding to α‐adrenergic receptors. In cortex, clonidine treatment increased the Bmax value of 3H‐spiroperidol binding to dopaminergic receptors. Clonidine treatment produced a decrease in the Bmax value in cortex while in hypothalamus and medulla, an increase in the Bmax value of 3H‐quinuclydinyl benzylate (QNB) binding to muscarinic receptors was observed. In medulla, clonidine treatment increased the Bmax value of 3H‐5‐hydroxytryptamine (HT) binding to 5‐HT1 receptors. No change was observed in dissociation constant (Kd) values of any 3H‐ligand in any brain region. In vitro studies showed interaction of clonidine with 3H‐dihydroergocryptine and 3H‐QNB. It can be concluded from the present study that chronic administration of clonidine produces an up‐regulation of α‐adrenergic, cholinergic (muscarinic), and serotonergic (5‐HT1) receptors in brain regions mainly involved in cardiovascular regulation.