By Gary C. Rosenfeld Ph.D., David S. Loose PhD
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Additional resources for BRS Pharmacology
Mechanism of action (Fig. 3A and B) a. Indirect-acting parasympathomimetic agents inhibit AChE and increase ACh levels at both muscarinic and nicotinic cholinoceptors to mimic many of the physiologic effects that result from increased ACh in the synaptic junction and stimulation of cholinoceptors of the parasympathetic division of the ANS. b. ACh interacts with AChE at two sites: The N1 of choline (ionic bond) binds to the anionic site, and the acetyl ester binds to the esteratic site (serine residue).
GI tract (1) Direct-acting muscarinic cholinoceptor agonists increase smooth muscle contractions and tone, with increased peristaltic activity and motility. (2) These drugs increase salivation and acid secretion. d. Urinary tract (1) Direct-acting muscarinic cholinoceptor agonists increase contraction of the ureter and bladder smooth muscle. (2) These drugs increase sphincter relaxation. e. Respiratory system effects of direct-acting muscarinic cholinoceptor agonists include bronchoconstriction with increased resistance and increased bronchial secretions.
Acetyl-serine is hydrolyzed to serine and acetate. The half-life (t1/2) of acetylserine hydrolysis is 100–150 microseconds. c. Edrophonium (Tensilon) acts at the same sites of AChE to competitively inhibit ACh hydrolysis. It has a short duration of action (5–15 min). d. Neostigmine (Prostigmin), physostigmine (Eserine, Antilirium), and demecarium (Humorsol), like ACh, interact with AChE and undergo a two-step hydrolysis. However, the serine residue of the enzyme is covalently carbamylated rather than acetylated.