Intravenous dose-response relationships were used to correlate neuromuscular paralysis with effects on autonomic mechanisms in anaesthetized cats. Whereas autonomic blockade with tubocurarine occurred at parasympathetic and sympathetic ganglia, neuromuscular paralysing doses of gallamine, alcuronium, pancuronium and fazadinium caused blockade at vagal postganglionic sites in the heart. The vagolytic (atropinic) activity of these compounds in cats relative to their neuromuscular blocking activity appeared to correlate well with their known liability to cause undesirable hypertension and tachycardia in man. The absence of cardiovascular effects after the administration of neuromuscular blocking doses of dimethyl tubocurarine would support its more extensive clinical use, but the need remains for a short-acting muscle relaxant with properties similar to those of dimethyl tubocurarine.