Preganglionic cervical and splanchnic sympathetic activity was recorded before and during administration of inhalation anaesthetics, in rabbits ventilated with oxygen and given gallamine. During control periods; when light anaesthesia was maintained with pentobarbitone, sympathetic discharge responded to changes in arterial pressure. Increased arterial Pco2 exaggerated the amplitude of the respiratory sympathetic rhythm, and had a more variable effect on the mean impulse discharge rate. Preganglionic activity was increased by 25–50 per cent cyclopropane, which usually raised arterial pressure; by halothane, which caused severe hypotension; and by diethyl ether, which produced smaller circulatory changes. These experiments question the concept of “central vasomotor depression” during inhalation anaesthesia in the rabbit.