The effect of Buthus occitanus venom on the isolated hearts appears to be mediated largely through stimulation of the autonomic nervous system with predominance of sympathetic stimulation and release of tissue catecholamines, although a direct cardiac stimulant action was also found. The injection of the venom into rabbits caused initial short lasting bradycardia followed by tachycardia then a prolonged bradycardia. The initial bradycardia was due to the cholinergic effect of the venom, the tachycardia to sympathetic stimulation and release of tissue catecholamines, while the delayed bradycardia seemed due to changes in the ionic composition of blood; notably hyperkalemia and hypocalcemia. The most striking electrocardiographic effects of the venom seemed related to inferior wall infarction and right bundle branch block. The former was evidenced from elevation of the ST segment in II, III and AVF and its depression in I, aVR, aVL and V1. The latter was revealed from the RSR′ pattern in V1. The wide S wave in I and V5, the prolonged QRS complex, the ST depression in V1 and the wide rSr′ complex in aVR. Some of the electrocardiographic wave abnormalities appeared to be mediated through hyperkalemia as shown from the tall, peaked and slender T wave and the wide QRS complex. The sympathetic stimulation and release of tissue catecholamines caused by the venom mask, while vagal stimulation potentiates, the effects due to electrolyte changes. The venom decreased the respiration rate but caused an increase in depth. The effect was greatly attenuated by carotid sinus and body denervation. The venom caused marked hypertension in cats, rats and guinea pigs. In cats blocking the alpha adrenergic receptors with phenoxybenzamine reversed the hypertensive effect of the venom to a hypotensive action that was blocked by propranolol. B. occitanus venom is unique among scorpion venoms in stimulating β-adrenergic receptors of the vascular system.