Category: MDG5238 (page 4 of 4)

VX Nerve Agent

VX nerve agent,  which has been in the news lately with the killing of Kim Jong-nam, is another example of an organophosphate anticholinesterase.

The newspapers and other media have recently reported that it was the VX nerve agent that was used to kill Kim Jong-nam, the half-brother of North Korea’s leader, in Malaysia. VX nerve agent is an example of an organophosphate anticholinesterase. Other examples of organophosphate anticholinesterases include the chemical weapon sarin and the organophosphate insecticides such as a malathion.

VX (S-2 Diisoprophylaminoethyl methylphosphonothiolate) is one of the most toxic nerve agent known. It is especially insidious as it is a highly viscous, tasteless and odourless liquid that can easily be transferred via clothing to be absorbed into the body by inhalation, ingestion, skin contact, or eye contact.

Although more potent and fast-acting, the effects of VX poisoning would be the same as for any organophosphate anticholinesterase. Inhibition of acetylcholinesterase will result in increased levels of acetylcholine at all cholinergic synapses in the body.

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Sympathetic cholinergic innervation of blood vessels? Not in humans.

Exceptions to the general rule that the sympathetic nervous system is adrenergic include cholinergic innervation of sweat glands expressing M3 receptors and dopaminergic innervation of the renal blood vessels expressing D1 receptors. But what about the arteries of skeletal muscle? 

Parasympathetic cholinergic fibres innervate some blood vessels. In arterial blood vessels, the release of acetylcholine activates M3 receptors on the vascular endothelium, which are coupled to formation of nitric oxide (NO) that produces vasodilation (1). However, if the synthesis of NO is inhibited, the activation of M3 and M2 receptors can produce vasoconstriction. In contrast, cerebral arteries express M5 receptors, which produce vasodilation in response to acetylcholine (1).

In cats and dogs, some of the arterial blood vessels in skeletal muscle are innervated by sympathetic cholinergic nerves that release acetylcholine, which acts at M3 receptors to produce vasodilation (1). In these species, the sympathetic nervous system innervation of the arterial blood vessel in skeletal muscle appears to play a role in active hyperaemia, increasing blood flow to the muscle at the start of exercise (1).

In contrast to cats and dogs, humans do not have sympathetic cholinergic innervation of arterial blood vessels in skeletal muscle (1).

Reference:
(1) Richard E Klabunde Cardiovascular Physiology Concepts: Adrenergic and Cholinergic Receptors in Blood Vessels http://www.cvphysiology.com/Blood%20Pressure/BP010b [Accessed 7 Feb 2017]

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