Abstract

SODIUM azide produces extrapyramidal symptoms with necrosis of the cerebral cortex, cerebellum, and basal ganglia. Toxicity with this metabolic inhibitor may also include hypotension, blindness and hepatic necrosis1–5. Many hormones and drugs mediate their effects by altering the intracellular levels of cyclic AMP and/or cyclic GMP6–10. We found that NaN3 increases cyclic GMP levels in incubations of slices from cerebral cortex, cerebellum or liver, and also stimulates guanylate cyclase activity. In contrast to other agents that can increase cyclic GMP accumulation in tissues the effect of NaN3 is observed in the absence of added calcium.

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