Some authors have shown that neurons can produce hydrogen cyanide upon activation of their opioid receptors by endogenous or exogenous opioids. They have also shown that neuronal production of HCN activates NMDA receptors and plays a role in signal transduction between neuronal cells (neurotransmission). Moreover, increased endogenous neuronal HCN production under opioids was seemingly needed for adequate opioid analgesia, as analgesic action of opioids was attenuated by HCN scavengers. They considered endogenous HCN to be a neuromodulator.
It has also been shown that, while stimulating muscarinic cholinergic receptors in cultured pheochromocytoma cells increases HCN production, in a living organism (in vivo) muscarinic cholinergic stimulation actually decreases HCN production.
Leukocytes generate HCN during phagocytosis, and can kill bacteria, fungi, and other pathogens by generating several different toxic chemicals, one of which is hydrogen cyanide.
The vasodilatation caused by sodium nitroprusside has been shown to be mediated not only by NO generation, but also by endogenous cyanide generation, which adds not only toxicity, but also some additional antihypertensive efficacy compared to nitroglycerine and other non-cyanogenic nitrates which do not cause blood cyanide levels to rise.
HCN is a constituent of tobacco smoke.