It was shown that "mouse" toxin of Yersinia pestis injected into the rat tail vein (LD100) caused a 2-fold decrease in the glycogen content in the liver and the glucose content in the blood. The Bmax of beta-adrenoceptors as well as basal, forskolin, 5-guanylyl imidodiphosphate, fluoride and glucagon-stimulated liver adenylate cyclase (AC) activities did not change in all periods of intoxication. After 5 hours of intoxication isoproterenol had no effect on AC; however, the cAMP content was increased 1.5 times in comparison with control. These data suggest that plague intoxication has no effect on cAMP-dependent regulation of glycogenolysis and gluconeogenesis in the liver. The action mechanism of toxin(s) on carbohydrate metabolism in also unrelated to the decrease in Bmax for alpha 1 adrenergic receptors in liver membranes, whose number increased 1.3 and 1.5 times after 1 and 2 hours of intoxication.