A class of autonomic drugs used for reversing skeletal muscle relaxation caused by a nondepolarizing blocker is the:

A nondepolarizing skeletal muscle blockade caused by antagonists such as d-tubocurarine is produced when these drugs pharmacologically antagonize acetylcholine and bind N2-nicotinic receptors of the motor end plate. This binding hyperpolarizes the muscle cell membrane. Reversal of a nondepolarizing block requires additional acetylcholine to compete with the neuromuscular blocking agent. Indirect acting cholinergic drugs such as cholinesterase inhibitors potentiate acetylcholine levels, resulting in a non selective mechanism of action at cholinergic receptors. It is the nicotinic action of acetylcholine at N2-nicotinic sites that is responsible for reversing a nondepolarizing neuromuscular block. Sympathomimetics and sympatholytics are ineffective in reversing non depolarizing blockade because there are no adrenergic nerves innervating skeletal muscle. (There are a few b2-adrenergic receptors located on skeletal muscle cell membranes. Stimulation of such adrenoceptors may result in skeletal muscle fasciculation, but would not be sufficient to reverse muscle paralysis caused by a nondepolarizing blocker.) Parasympatholytics (also known as muscarinic antagonists) have no effect at the neuromuscular junction because muscarinic receptors are not found at such locations. Ref: Taylor P. (2011). Chapter 10. Anticholinesterase Agents. In L.L. Brunton, B.A. Chabner, B.C. Knollmann (Eds), Goodman & Gilman's The Pharmacological Basis of Therapeutics, 12e.