The exact mechanism of the toxicity of sodium azide remains unknown. In 1955, Robertson and Boyer postulated that the inhibition of heme-type enzymes,
such as catalase, peroxidase, and cytochrome oxidase, was metabolically responsible for its toxicity (Robertson and Boyer 1954; Trochimowicz 1990).
Later, Smith et al. showed that it was unlikely that this metabolic mechanism accounted for its lethality (Smith et al. 1991). Subsequently, Smith et
al. showed that enhanced excitatory transmission in the central nervous system after conversion of sodium azide to nitric oxide was a more likely
explanation for its lethality (Smith and Wilcox 1994). They explained lethality as a neurotransmitter effect rather than a metabolic effect. In the
cardiovascular system, stimulation of carotid body chemoreceptors, stimulation of cardiac muscle, or dilation of coronary vessels may account for the
hypotensive effect of sodium azide. Sodium azide produces tachycardia (rapid heart beat) centrally rather than by carotid sinus reflex response to
falling blood pressure (Trochimowicz 1990; Smith and Wilcox 1994; Smith et al. 1991).
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