Adverse Effects

Potentially severe adverse effects can result from systemic administration of cholinomimetic drugs, and none should be administered by intramuscular or intravenous injection. If significant amounts of these drugs enter the circulation, nausea, abdominal cramps, diarrhea, salivation, hypotension with reflex tachycardia, cutaneous vasodilation, sweating, and bronchoconstric-tion can result. Pilocarpine can cross the blood-brain barrier and affect cognitive function. Even the topical application of cholinomimetics to the eyes can present some risk, and the escape of cholinomimetics into the circulatory system following topical application to the eye can be minimized by pressure applied to the lacrimal duct. Within the eye, cholinomimetics elicit miosis and spasm of accommodation, both of which disturb vision.

Bethanechol is relatively selective in activating choli-noreceptors in the gastrointestinal and urinary tracts when taken orally, but it is less selective when given sub-cutaneously, and it is very dangerous when given intramuscularly or intravenously, having the potential to produce circulatory collapse and cardiac arrest. Systemic poisoning with cholinomimetics can be treated with the muscarinic receptor antagonist atropine.

Bethanechol should not be used in patients with possible mechanical obstruction of the bladder or gastrointestinal tract or when contraction of smooth muscles in these tissues may be harmful (e.g., recent intestinal resection). It is also contraindicated in patients with bronchial asthma, peptic ulcer disease, coronary artery disease, gastrointestinal hypermotility or inflammatory disease, hypotension or marked bradycardia, hyperthy-roidism, parkinsonism, or epilepsy. Care should be exercised in administering pilocarpine to elderly patients because it can enter the CNS and affect memory and cognition, even when applied topically to the eye.

sis of ACh, but they differ markedly in their pharmaco-kinetic properties.

Inhibition of AChE can increase the stimulation of both muscarinic and nicotinic receptors produced by synaptically released ACh. Nicotinic receptors can also be stimulated directly by AChE inhibitors with a quaternary ammonium group, and this can potentiate their cholinomimetic effect. Finally, although inhibition of true AChE is most important for potentiating the synaptic activity of ACh, several AChE inhibitors also inhibit the pseudo-ChE in plasma. This can permit plasma concentrations of ACh to rise markedly and activate endothelial muscarinic receptors.

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