The biological effect of purified beta toxin of Clostridium perfringens type C in vivo was investigated. After intravenous injection of the purified beta toxin into rats, a rise in blood pressure and a simultaneous fall in heart rate were observed. After the blood pressure reached a maximum, the heart rate recovered gradually, and electrocardiographic and respiratory changes began. The rise in blood pressure induced by beta toxin tended to be proportional to the amount of toxin. The latent period between the injection of toxin and the onset of the increase, and also the time between the injection and the maximum pressure induced by the toxin decreased with increasing concentration of the toxin. A good correlation was found between the factor producing the rise in blood pressure and beta toxin. Alpha adrenergic and ganglionic blocking agents reduced blood pressure levels elevated by beta toxin. The data suggest that the toxin causes a release of catecholamines, and that the increase in blood pressure was induced by released catecholamines.Clostridium perfringens type C produces beta toxin, which is lethal and nonhemolytic and, after intradermal inoculation, produces necrotic lesions in guinea pigs. Previously we reported the extensive purification of beta toxin produced by C. perfringens type C (9), and suggested that the purified toxin is a thermolabile protein (10) and similar to oxygen-labile toxins produced by other bacteria in being inactivated by oxidizing reagents and activated by reducing reagents (II). Beta toxin produced by C. perfringens type C has been thought to be closely correlated with necrotic enteritis of animals and man (2,4,5,8,14). The diseases are characterized by acute sudden onset, hemorrhagic enteritis, severe hemorrhage into the lumen of the small intestine, and early death. However, little can be said concerning the role of the toxin in the pathogenesis of the disease. To study the mode of action of the toxin, it is important to determine the biological effect of the purified beta toxin in vivo. In the present paper, we describe the effect of beta toxin on blood pressure, heart rate, cardiogram, and respiration in rats.