Relationship of stress-induced histidine decarboxylase to circulatory homeostasis and shock.

Histidine decarboxylase activity of mouse tissues is increased by stress and by injection of epinephrine and norepinephrine, suggesting a balance between histamine and catechol amines producing a component of circulatory homeostasis. Imbalance during intense stress might lead to failure of circulatory homeostasis and to shock. Reasons for discounting histamine as "shock toxin" may be invalid.