One approach to lessening the impact of these abnormalities is to inhibit the breakdown of acetylcholine (Ach) by blocking the relevant enzyme AchE (acetyl choline esterase) [2](Figure 1).
Synaptic transmission from a nerve cell to another cell such as a muscle cell in many situations relies on acetyl choline. The enzyme acetylcholinesterase in nerve endings catalyses the hydrolysis of acetylcholine to choline and acetylCoA, thus determining a very short action of acetylcholine.
It is in high concentration in the electric organ of the electric eel, Eletrophorus Electricus, an adaptation of a synaptosome that depends on acetyl choline as the neurotransmitter.
Tiotropium produces relaxation of airway smooth muscle by antagonism of acetyl choline at M3-muscarinic receptors, while formoterol achieves that effect through stimulation of [[beta].sub.2] receptors, which results in an increase of cyclic adenosine monophosphate (Chest 2004; 125:249-59).
Simply put, atropine reverses the effects of acetyl choline, the neurotransmitter secreted by nerves like the vagus nerve, that acts to slow the heart rate, among many other activities.