Organophosphate and carbamates are AchE inhibitor, so they should increase Ach and cause muscle contraction at NMJ. How come overdoses of OP and carbamate (ie nerve gas and insecticide) can cause muscle weakness and respiratory paralysis?
AchE inhibitors such as organophosphates and the carbamates cause increased levels of Ach at all sites that release Ach (ie. all ganglia, the NMJ, the parasympathetic neuroeffector site, sweat glands). This means they can have widespread actions on the autonomic nervous system (both divisions) and the somatic nervous system. At high doses the muscle weakness and respiratory paralysis is due to depolarizing block at the NMJ on the Nm-receptor (similar to the actions of succinylcholine). Question: (1) Pirenzepine is an M1 selective antagonist, why is it used for peptic ulcers? Is M1 block specifically linked to a decrease in gastric secretions. (2). Can you explain how an ACHe inhibitor (i.e., benztropine) is used for the treatment of parkinson’s? Answer: (1). Yes, activation of M1-receptors increase gastric acid secretion. (2). Benztropine is a muscarinic antagonist not a AchE inhibitor. Parkinsons D. is associated with decreased central dopamine function and increased cholinergic activ
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