BETA-ADRENOCEPTOR EXPRESSION ON CIRCULATING MONONUCLEAR-CELLS OF IDIOPATHIC PARKINSONS-DISEASE AND AUTONOMIC FAILURE PATIENTS BEFORE AND AFTER REDUCTION OF CENTRAL SYMPATHETIC OUTFLOW BY CLONIDINE

There is a short-term up-regulation of beta-adrenoceptors on periphera l blood mononuclear cells (PBMC) after reduction of central sympatheti c outflow by clonidine in normal individuals. We have studied beta-adr enoceptor number and affinity on PBMC in idiopathic Parkinson's diseas e (PD), pure autonomic failure (PAF), and multiple system atrophy (MSA ; Shy-Drager syndrome) patients and age- and sex-matched normal contro ls (NC) before and after intravenous administration of clonidine, an a lpha2-adrenoceptor agonist which lowers blood pressure predominantly b y reducing CNS sympathetic outflow. Basal beta-adrenoceptor density wa s high in PAF but within the normal range in PD and MSA patients. Afte r clonidine there was a decrease in plasma levels of noradrenaline (NA ) and adrenaline (Ad) in PD, MSA, and NC, and an increase in growth ho rmone (GH) in PD, PAF, and NC. In PAF, NA and Ad remained unchanged. I n MSA, there was no increase in GH levels. There was an up-regulation of beta-adrenoceptors on PBMC at 30 and 60 minutes after clonidine adm inistration, which returned to baseline values after 2 hours, and the affinity of the receptors was decreased in NC and PD patients. Intrace llular production of cAMP after isoproterenol stimulation demonstrated that the up-regulation was not functional. Up-regulation after clonid ine did not occur in PAF and MSA patients. The observed correlation of plasma NA and sympathetic defect with basal and clonidine-induced up- regulation of beta-adrenoceptors on PBMC may provide insight into beta -adrenoceptor changes in other tissues and also help in differentiatin g subgroups of autonomic failure patients.