Abstract The aim of this investigation in anaesthetized dogs was to provide direct evidence for an activation of the sympathetic nervous system by the muscarinic agonist talsaclidine (WAL 2014 FU). Intravenous infusion at a rate of 1 mg kg/min increased plasma catecholamines and in particular epinephrine, thus indicating a predominant stimulation of the adrenals. Sympathetic activation was also indicated by increases in renal vascular resistance, an effect which was sensitive to α-adrenolysis. It is concluded that the sympathetic activation by talsaclidine is due to full agonism at the M 1-receptor and the ability to cross the blood-brain barrier. As talsaclidine is less potent and only a partial agonist at M 2- and M 3-receptors many peripheral actions mediated by these receptor subtypes are functionally antagonized by the concomitant sympathetic activation.